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Long-term carbon dioxide toxicity and climate change: a major unapprehended risk for human health

Authors:

Abstract

As atmospheric levels of carbon dioxide continue to escalate and drive climate change, the safe level for breathing is not clear. The toxicity of CO2 has been defined for short-duration exposures at high concentrations but it is unknown what levels will compromise human health when individuals are perpetually exposed for their lifetime. There is now substantial evidence that permanent exposure, to CO2 levels predicted in the future, will have significant effects on humans. Blood CO2 levels in populations are increasing and unhealthy concentrations have been measured from people in common indoor environments where reduced thinking ability and health symptoms have been observed at levels of CO2 above 600 ppm for relatively short-term exposures. Although humans and animals are able to deal with elevated levels of CO2 in the short-term due to compensation mechanisms in the body, the eventual failure of these may have severe consequences in a perpetual environment of elevated CO2. Protein malfunctions in cells due to elevated CO2 and associated low pH has the potential to cause threats to life including cancer, neurological disorders, lung disease, diabetes, etc. In particular excess CO2 causes the overexpression of carbonic anhydrase, the enzyme that catalyses CO2 in the body, causes calcification in the kidneys, arteries and tissues, along with other diseases and this may be an existential threat. Although there is very low awareness of this risk and its proximity is yet to be adequately defined, it is likely that human health will be significantly affected in the near future with the progressive severity dependant on CO2 emissions.
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Long-term carbon dioxide toxicity and climate change: a major
unapprehended risk for human health.
P.N. Bierwirth, PhD
Emeritus Faculty
Australian National University
First draft - Web Posted 25 February, 2014
Current Version – 8 April, 2022
ResearchGate DOI:10.13140/RG.2.2.16787.48168
Abstract
As atmospheric levels of carbon dioxide continue to escalate and drive climate change, the safe level
for breathing is not clear. The toxicity of CO2 has been defined for short-duration exposures at high
concentrations but it is unknown what levels will compromise human health when individuals are
perpetually exposed for their lifetime. There is now substantial evidence that permanent exposure,
to CO2 levels predicted in the future, will have significant effects on humans. Blood CO2 levels in
populations are increasing and unhealthy concentrations have been measured from people in
common indoor environments where reduced thinking ability and health symptoms have been
observed at levels of CO2 above 600 ppm for relatively short-term exposures. Although humans and
animals are able to deal with elevated levels of CO2 in the short-term due to compensation
mechanisms in the body, the eventual failure of these may have severe consequences in a perpetual
environment of elevated CO2. Protein malfunctions in cells due to elevated CO2 and associated low
pH has the potential to cause threats to life including cancer, neurological disorders, lung disease,
diabetes, etc. In particular excess CO2 causes the overexpression of carbonic anhydrase, the enzyme
that catalyses CO2 in the body, causes calcification in the kidneys, arteries and tissues, along with
other diseases and this may be an existential threat. Although there is very low awareness of this
risk and its proximity is yet to be adequately defined, it is likely that human health will be
significantly affected in the near-future with the progressive severity dependant on CO2 emissions.
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1. Introduction
An axiom of modern science, as quoted from TS Huxley, is “do not pretend that conclusions are
certain which are not demonstrated or demonstrable”. Carbon dioxide is one of the most frequently
overlooked of all toxic gases. Even to refer to CO2 as a toxic gas is a surprise to many safety
professionals (Henderson 2006). In indoor environments CO2 concentration is often elevated relative
to ambient outdoor levels due to the fact that the exhaled breath from humans contains high CO2
(about 4%) and ventilation may not be adequate to prevent the resulting increase in CO2. Despite
the possible adverse effects on health where many people occupy buildings or vehicles, there is very
little awareness of this issue in the general community.
The average ambient concentration of CO2 (in fresh air) has been rapidly increasing and is recently
around 410 ppm (Scripps Institution of Oceanography 2020; Schmidt 2020) (Figure 1). This increase
is due to humanity’s activities, largely resulting from the burning of fossil fuels (Eggleton 2013).
Figure 1. The atmospheric carbon dioxide concentrations (in ppm) over the last 2000 years, based on
measurements of air trapped in Antarctic ice, shown in blue-grey diamonds, and the modern Cape
Grim, Tasmania direct air measurements, shown in orange. (From Schmidt 2020).
Very early primate ancestors of humans were evolving around 23 million years ago. Throughout all
of the ensuing period of human evolution it is clear that levels of CO2 in the ambient atmosphere
remained relatively stable at below or close to 300 parts per million (ppm), this being derived from a
combination of studies of relict features including air trapped in ice cores (Schmidt 2020), the
composition of fossil plankton (Zachos et al. 2001) and Carbon-13 (13C) content in fossil plant
material (Cui et al. 2020). Since about 1820, CO2 levels have increased rapidly and are now above
400 ppm (Figure 1). This is a potentially catastrophic problem for many species of animals, including
humans, for a number of reasons. The most well publicised issue is that of climate change. The
mechanisms and history of global warming associated with CO2 increase are well understood and
the increase in atmospheric energy gradients will produce more extreme temperatures and weather
events. To many people, climate change itself may not appear to be catastrophic – for example it
might be possible to escape the effects of even a 5 degree C increase this century by moving to a
cooler and safer geographic location. However, it is possible that humans have overlooked the more
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direct and immediate toxicity aspect of increasing atmospheric CO2. The earth’s atmosphere has
already reached CO2 levels that are outside the range breathed by humans throughout their
evolution. As well, in earlier pre-primate epochs, the effect of elevated atmospheric CO2 causing
physiological stress, has been postulated to be a cause of mass extinction events (Knoll et al. 1996)
We know that breathing CO2 is toxic to humans when levels are high with numerous deaths reported
based on occupational exposure (Scott et al. 2009). Although the CO2 exposure limit for an 8-hour
working day has been set at 5,000 ppm (OSHA 2012), this limit was decided in 1946 and based on
relatively short-term observations of fit and healthy submariners (Scott et al, 2009). The safe level
for lifetime exposure may be significantly lower than this and a number of researchers suggest there
could be toxicity effects at CO2 levels predicted in the near future with ongoing anthropogenic
emissions (Portner et al. 2004; Robertson 2006; Ezraty et al. 2011; Antic 2012; McNeil and Sasse
2016; Karnauskas et al. 2020). So the question is: how long will it take, at present and future rates of
increase, to reach levels that will impact on human health (no matter where you live) over a
lifetime? To answer this question, the safe level of CO2, for continuous breathing in humans, needs
to be determined. This paper is an attempt to evaluate available knowledge and to examine the
likely and possible risks (for the near to medium-term future).
2. The role of carbon dioxide in breathing
Breathing is one part of physiological respiration and is required to sustain life (Raven et al.
2007). Aerobic organisms like birds, mammals, and reptiles, require oxygen to release energy by
cellular respiration, through the metabolism of molecules such as glucose. During aerobic
respiration, glucose is broken down by oxygen to release energy, while carbon dioxide and water are
the by-products of the reaction. Breathing delivers oxygen to where it is needed in the body and
removes carbon dioxide thereby exchanging oxygen and carbon dioxide between the body and the
environment. Carbon dioxide (CO2) is essentially a waste product and needs to be removed from our
body. CO2 from respiring tissues enters the blood plasma and diffuses into the red cells, where it is
rapidly hydrated to H+ and bicarbonate (HCO3-) by the enzyme carbonic anhydrase (CA) (Arlot et al.
1985; Adeva-Andany et al. 2014). This enzyme enables the breakdown of CO2 which returns to the
plasma as bicarbonate and is then transported to the lungs (Adeva-Andany et al. 2014). When the
bicarbonate reaches the lungs, CA in the alveoli catalyses the reverse reaction generating water and
carbon dioxide which is exhaled as a gas. CA thus allows a large pool of otherwise slowly reacting
plasma HCO3- to be utilized in CO2 excretion (Arlot et al. 1985).
There is an optimal range for the concentrations of CO2 in the air we breathe. Too little can mean
that breathing is too slow and not enough oxygen is brought into the body (Patton and Thibodeau
2009). Too much can compromise our ability to remove CO2 (from our bodies) as a waste product. So
what are the effects of too much CO2 and what is the level that can cause health problems (in
humans)?
3. Health effects from short term exposure to high levels of CO2
Breathing too much CO2 results in high levels of CO2 in the blood (hypercapnia) associated with a
decrease in blood pH (increased acidity) resulting in a condition known as acidosis. The decreases in
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blood and tissue pH produce effects on the respiratory, cardiovascular, and central nervous systems
(CNS) (Eckenhoff and Longnecker 1995). Changes in pH act directly and indirectly on those systems
producing effects such as tremor, headache, hyperventilation, visual impairment, and CNS
impairment. In terms of worker safety, the US Occupational Safety and Health Administration has set
a permissible exposure limit (PEL) for CO2 of 5,000 parts per million (ppm) (or 0.5 %) over an 8-hour
work day (OSHA 2012). They report that exposure to levels of CO2 above this can cause problems
with concentration, an increased heart rate, breathing issues, headaches and dizziness.
Exposures to 1-5 % CO2 for short-term periods have been documented to produce symptoms on
humans and animals such as dyspnea (shortness of breath), modified breathing, acidosis, tremor,
intercostal pain, headaches, visual impairment, lung damage, increased blood pressure, bone
degradation, reduced fertlity, alterations to urine and blood chemistry as well as erratic behaviour
(Halperin 2007; Rice 2004; Guais et al. 2011; Schaefer et al. 1963; Yang et al. 1997). These levels of
CO2 also induce panic attacks, interrupt the processes of metabolic enzymes and disrupt normal cell
division processes (Colasanti et al. 2008; Guais et al. 2011; Abolhassani et al. 2009).
Health risks continue to escalate, with progressively higher CO2 concentrations causing more severe
reactions and faster responses. A value of 40,000 ppm is considered immediately dangerous to life
and health given that a 30-minute exposure to 50,000 ppm produces intoxication, and
concentrations around 70,000 ppm produce unconsciousness (NIOSH 1996). Additionally, acute
toxicity data show the lethal concentration for CO2 is 90,000 ppm (9%) for a 5 minute exposure.
There are indoor situations where exhaled human breath and restricted air flow can produce
extreme and dangerous levels of CO2. For example infant deaths have been associated with levels of
up to 8% (80,000 ppm) CO2 for an infant covered by blankets (Campbell et al. 1996).
4. Physiological compensation for elevated CO2
When considering long-term effects of breathing sustained elevated CO2, it is important to consider
compensation mechanisms in the body, that regulate for increased CO2 and acidity in the blood, and
how these change over time with persistent exposure. The lowering of blood pH triggers various
compensatory mechanisms, including pH buffering systems in the blood, increased breathing to
reduce excess CO2 in the bloodstream, increased excretion of acid by the kidneys to restore acid-
base balance, and nervous system stimulation to counteract the direct effects of pH changes on
heart contractility and vasodilation (widening of the blood vessels) (Burton 1978; Eckenhoff and
Longnecker 1995). In respiratory acidosis, for a period the kidneys retain bicarbonate helping to
normalise the pH of the blood as it passes through them. This occurs within 6 to 8 hours of exposure
but achieves full effect only after a few days. With continued high levels of CO2 in the blood,
metabolic acidosis occurs and the kidneys do not respond in producing bicarbonate (Schaefer et al
1979a). After this the body uses the bones to help regulate the acid levels in the blood. Bicarbonate
and a positive ion (Ca2+, K+, Na+) are exchanged for H+. The kidneys are involved in a wider array of
physiological compensation responses to CO2 induced pH imbalance (acidosis). The kidney tubule
recovers filtered bicarbonate or secretes bicarbonate into the urine to help maintain acid-base
balance in the blood and this again involves the CA enzyme (Adeva-Andany 2014).
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5. Health effects at common indoor CO2 concentrations
5.1 Classrooms
There is a large volume of recent literature that has documented the occurrence and levels of CO2 in
classrooms across the world including kindergartens, day-care centres, primary schools, high schools
and universities (Bako-Biro et al 2011; Widory and Javoy 2003; Kukadia et al. 2005; Dijken et al.
2005; Branco et al. 2015; Heudorf et al. 2009; Santamouris et al. 2008; Ferreira and Cardoso 2014;
Gaihre et al. 2014; Jurado, et al. 2014; Lee and Chang 2000; Muscatiello et al 2015; Carreiro-Martins
et al. 2014). There is general agreement that the levels of CO2 in 20-50% of classrooms commonly
exceed 1,000 ppm and are often much higher, sometimes reaching levels as high as 6000 ppm for
extended periods. A number of studies have identified CO2 associated symptoms and respiratory
diseases such as sneezing, rales, wheezing, rhinitis, and asthma (Carreiro-Martins et al. 2014;
Ferreira and Cardoso 2014). Other symptoms; i.e. cough, headache, and irritation of mucous
membranes, were also identified (Ferreira and Cardoso 2014). Lack of concentration was associated
with CO2 levels above 1000 ppm. Gaihre et al. (2014) found that CO2 concentrations exceeding 1000
ppm is associated with reduced school attendance. Teachers also report neuro-physiologic
symptoms (i.e., headache, fatigue, difficulty concentrating) at CO2 levels greater than 1000 ppm
(Muscatiello et al. 2015).
5.2 Offices
Offices have levels of CO2 similar to classrooms depending on the number or density of workers and
the types of ventilation systems (Lu et al. 2015; Tsai et al. 2012, Seppanen et al. 1999). These studies
have found strong evidence of the relationship between CO2 levels in offices and Sick Building
Syndrome (SBS) health effects such as headaches, dizziness, fatigue, respiratory tract symptoms, eye
symptoms, nasal and mucous membrane symptoms (Seppanen et al. 1999; Lu et al. 2015; Tsai et al.
2012; Vehviläinen et al. 2016; MacNaughton et al. 2016). Seppanen et al. (1999) conducted a review
of available literature and were careful to eliminate other confounding airborne building
contaminants. The reviewed studies included over 30,000 human subjects, and they concluded that
the risk of SBS symptoms decreased significantly with carbon dioxide concentrations below 800
ppm. Whether CO2 itself is responsible for the health symptoms is still a subject of debate since
historically it has been assumed, despite lack of direct evidence, that other airborne contaminants
are the cause (Zhang et al. 2017).
More recently a number of studies have demonstrated that CO2 has direct impacts on human
physiology at levels commonly found in indoor environments (Azuma et al . 2018). Symptoms such
as fatigue and drowsiness caused directly by CO2 have been demonstrated by the use of
electroencephalogram (EEG) techniques (Snow et al. 2018; Pang et al. 2020). In a study of office
workers, a 20% increase in blood CO2, to significantly above normal levels, was measured along with
sleepiness, headaches, heart rate variation and poor concentration in air that averaged 2,800 ppm
CO2 (Vehviläinen et al. 2016) while lowered heart rate and arousal level (fatigue) is clear at 4000
ppm (Xia et al. 2020). Measurements of end-tidal PCO2 show a significant increase of CO2 in human
blood during tests conducted on astronauts after 4 months continually exposed to about 5,000 ppm
(Hughson et al. 2016). Increases in blood CO2 were associated with restricted lung function at levels
between 2,000 and 3000 ppm CO2 (Shriram et al. 2019). Zheutlin et al. 2014 used statistical data to
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determine an increasing trend in the average levels of CO2 in the blood for a national sample of
5,000 people from 1999 to 2012. Heart rate variation at 2700 ppm is confirmed by Snow et al. (2019)
for 10 minute exposure. MacNaughton et al. (2016) found that a 1,000 ppm increase in CO2 from
background levels was associated with a 2.3 bpm increase in heart rate after adjusting for potential
confounders. Another older study (Goromosov 1968) reported harmful physiological effects on
humans at only 1,000 ppm CO2 with changes in respiration, circulation, and cerebral electrical
activity. These physiological effects are being observed at much lower levels of CO2 than previously
anticipated (Azuma et al. 2018).
5.3 Vehicles
Although rarely studied for health effects, vehicles can often contain even higher levels of CO2
particularly where there are multiple passengers for relatively long journey times. CO2 levels can
build up to 5,000 ppm after less than an hour of driving with two people in a car with only internal
air (Gładyszewska-Fiedoruk 2011). With five people in a car with recirculated air levels of CO2 can
exceed 10,000 ppm (1%) after only 28 minutes, this being a level that is known to result in
respiratory acidosis (Constantin et al. 2016). Buses with high numbers of passengers consistently
reach average CO2 concentrations of > 2500 ppm (Chiu et al 2015). Airliners can contain levels of
around 2000 ppm for the duration of the flight (Gładyszewska-Fiedoruk 2012). Measurements on an
Italian submarine showed a steady increase to 5000 ppm CO2 after 2 hours of being submerged
(Ferrari et al. 2005). Extremely high CO2 concentrations (10,000-20,000 ppm) are commonly found
inside motorcycle helmets in both stationary and moving situations (Bruhwiler et al. 2005).
5.4 Mental impairment in indoor environments
There is now a significant body of research studies involving the detrimental effect of CO2 on
learning and cognitive abilities in humans at common indoor concentrations (Du et al. 2020). Testing
of students has found that CO2 can negatively affect attention, memory, concentration and learning
ability impacting on academic performance (Bako-Biro et al. 2011; Coley et al. 2007). Several recent
university studies of cognitive effects of CO2 have been notable in their strong research design
(Satish et al 2012; Allen et al 2016; Allen et al 2018; Scully et al 2019) with the testing environments
injected with pure CO2 meaning that the analysis of CO2 effects was not confounded by the presence
of other substances. These studies showed that low level CO2 (between 950 ppm and 2500 ppm CO2)
affected the cognitive abilities of students, information professionals and pilots in the indoor
environment. Satish el al. (2012) tested only variations in CO2 over periods of 2.5 hours of exposure.
For seven of nine scales of decision-making performance (basic activity, applied activity, task
orientation, initiative, information usage, breadth of approach, and basic strategy), performance was
significantly impaired in a dose-response manner with higher CO2 levels. For example, compared
with mean raw scores at 600 ppm CO2, mean raw scores at 1,000 ppm CO2 were 11–23% lower, and
at 2,500 ppm CO2 were 44–94% lower. As part of a larger study that included volatile organic
compounds (VOCs), Allen et al. (2016) found that, after CO2was independently modified (from a
baseline of 480-600 ppm) for individual 8 hour exposures, cognitive function scores were 15% lower
at 950 ppm and 50% lower at 1400 ppm. This study used similar methodology to score cognitive
function and the results largely repeated the findings of the earlier work (Satish et al 2012). However
one difference was that, at 1500 ppm CO2, even focussed activity was found to have declined (Allen
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et al 2016). In a study of pilots’ performance, Allen et al. (2018) found that negative impacts on
cognitive function were observed between 700 ppm and 1500 ppm CO2. Another study found similar
negative effects on human cognitive abilities, in experiments involving 140 minute sessions, as well
as increased fatigue at levels of 3000 ppm CO2 compared with 600 ppm (Kajtar and Herczeg 2012).
This study also measured some physiological parameters with heart rate analysis suggesting
significantly increased mental effort at 3000-4000 ppm.
Cognitive and neurological effects are also observed in animal studies. Mice exposed from birth to
1,000 ppm CO2 for 38 days had decreased Insulin-like Growth Factor-1 (IGF-1) which resulted in
greater anxiety and reduced cognitive function (Kiray 2014). Neurons were reduced in number and
were malformed at this CO2 level for several areas of the brain, with the largest effect for those areas
associated with learning and memory. Mice exposed to only 890 ppm from preconception to 3
months of age showed increased corticosterone levels in the blood and brain (Wyrwoll et al 2022).
Chronic elevation of brain corticoids associates with cognitive impairment and could harm the
developing brain (Stolp 2022).
5.5 Sleep impacts
Sleep quality is reduced at 1900 ppm CO2 when compared to 800 ppm in both subjective indices and
electroencephalogram (EEG) measurements of brain activity (Xu et al. 2020). When CO2 in arterial
blood rises to a certain extent, it will produce carbon dioxide narcosis respiratory inhibition,
weakened respiration, and hypoxia of human cells resulting in poor sleep quality (Xu et al. 2020).
Another example is people affected by sleep disordered breathing (SDB). Brillante et al (2012) found
that the development of nocturnal hypercapnia in normal indoor CO2 air concentration, quantitated
by a large difference in carbon dioxide in the blood between morning and evening, predicted
increased mortality in SDB patients. This is a result of the lack of efficacy of an individual’s
respiratory regulatory system in sleep for maintaining normal blood gas tensions (Brillante et al.
2012). As CO2 levels in the atmosphere increase into the future, the impacts on and number of
affected individuals will logically increase.
6. Health effects from long term exposure to elevated CO2 levels below 1%
Where indoor levels of CO2 are relatively high and affecting health, it is generally possible to obtain
relief by going outdoors. However this may not be the case in a climate change future where
ambient CO2 is persistently high and effects of continuous long-term exposure must be considered.
There have been very few studies related to long-term exposure at lower CO2 levels, elevated above
ambient, perhaps for logistical reasons since it is difficult to arrange an experiment for relevantly
long timeframes. We are looking for information on the effect on humans of CO2 levels at 1,000
ppm or less – noting that this is the level that some feasible models predict could be reached in the
ambient atmosphere in less than 100 years (Smith and Woodward 2014). Given the lack of research
at these CO2 levels, it seems reasonable to examine the research available for medium-term studies
on levels of CO2 less than 10,000 ppm (1%). Table 1 provides a summary of health effects, found in
the published literature and discussed in this paper, resulting from breathing CO2 at levels at or
below 1%.
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Table1. Documented health effects from breathing CO2 at concentrations at or below 1%.
CO2 Level Health effect Exposure Source
10,000 ppm
(1%)
Kidney calcification, decreased bone formation and
increased bone resorption in guinea pigs
6 weeks Schaefer et al., 1979a
10,000 ppm
(1%)
Cognitive impairment, increased diastolic blood
pressure
75 min Tu et al. 2020
8500 ppm Increased lung dead space volume 20 days Rice 2004
7000 ppm
(0.7%)
35% increase in cerebral blood flow (implications for
cognitive effects seen in other studies)
23 days Sliwka et al. 1998
5000-6600
ppm
Headaches, lethargy, moodiness, mental slowness,
emotional irritation, sleep disruption
Short-term Chronin et al. 2012; Law et
al. 2010
5000 ppm Kidney calcification, bone degradation in guinea pigs 8 weeks Schaefer et al 1979b
5000 ppm Elevated blood CO2 levels in astronauts 4 months Hughson et al. 2016
5000 ppm Current allowable levels for continuous exposure in
submarines and spacecraft
Operational
continuous
Halperin et al. 2007; Chronin
et al 2012
5000 ppm Permissible exposure limit (PEL) for a work day 8 hours OSHA 2012
5000 ppm Vascular and neurological changes 1.5 minutes Bright et al. 2020
4000 ppm Increase in heart rate, lowered arousal level/
increased fatigue and sleepiness
17 minutes Xia et al. 2020
3500 ppm Cognitive impairment, reduced human vigilance
(increased sleepiness)
4 hours Pang et al. 2020, Zhang et
al. 2020
3000 ppm Cognitive impairment, anxiety, neural damage,
oxidative stress in mice
38 days Kiray et al. 2014
3000 ppm Systemic inflammation and physiological stress in
rodents
9-13 days Beheshti et al. 2018
2700 ppm Drowsiness measured by EEG 10 min Snow et al. 2018
2700 ppm Increase in heart rate 10 min Snow et al. 2019
2000-4000
ppm
Unhealthy blood CO2 levels - 15% above normal
range, sleepiness, headaches, heart rate variations
4 hours Vehviläinen et al. 2016
2000-4000
ppm
Inflammation and vascular damage in mice 2 hours Thom et al.2017
2000-3000 Restrictive lung behaviour and elevated blood CO2 3 hours Shriram et al. 2019
9
ppm
2000 ppm Kidney effects in animals (likely calcification) -
incomplete study
Chronic
studies
Schaefer 1982
1900 ppm Reduced sleep quality, drowsiness 8 hours Xu et al. 2020
1400-3000
ppm
Significant impairment of cognitive function
including fatigue
2.5 to 8
hours
Satish et al 2012; Allen et al
2016; Kajtar & Herczeg 2012
1200 ppm Reduced cognitive function 2.5 hours Scully et al. 2019
1000 ppm Harmful changes in respiration, circulation, and the
cerebral cortex
A short time Goromosov 1968
1000 ppm Oxidative stress and damage to DNA in bacteria
(implications for cancer diseases in humans)
3 hours Ezraty et al. 2011
1000 ppm Cognitive impairment, anxiety, neural damage,
oxidative stress in mice
38 days Kiray et al. 2014
1000 ppm Level associated with respiratory diseases,
headache, fatigue, difficulty concentrating in
classrooms
Short-term Carreiro-Martins et al. 2014;
Ferreira and Cardoso 2014;
Seppanen et al. 1999
950-1400
ppm
Health symptoms (respiratory, skin, eyes, headaches,
cognitive, dizziness, sensory), increase in heart rate
30 min MacNaughton et al. 2016
950-1000
ppm
Moderate impairment of cognitive function 2.5 to 8
hours
Satish et al 2012; Allen et al
2016; Allen et al 2018
890 ppm Impaired lung function in new-born female mice,
slightly lower blood pH. Reduced growth,
hyperactivity, increased stress hormone associated
with cognitive impairment
3 months Larcombe et al. 2021;
Wyrwoll et al. 2022
800 ppm Level associated with Sick Building Syndrome -
headaches, dizziness, fatigue, respiratory tract, eye,
nasal and mucous membrane symptoms
Short-term Seppanen et al. 1999; Lu et
al. 2015; Tsai et al. 2012
700-900 ppm Gastropods: reduced growth, reduced food
absorption and oxygen uptake, reproductive failure
6-10 months Navarro et al. 2022;
Mardones et al. 2022
700 ppm Modification of behaviour, stress hormone and
respiratory muscle structure in rats
15 days,
6hrs/day
Martrette et al. 2017
400 ppm Current average outdoor air concentration - no
known effect
Lifetime Carbon Dioxide Information
Analysis Center 2015
280-300 ppm Pre-industrial outdoor level from about 1820 to at
least 25 million years ago - no effect
Lifetime Beerling and Royer 2011;
Zachos 2001.
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6.1 Spacecraft
A good information source may be the safety guideline documents for activities where humans are
required to remain in enclosed spaces for long periods such as spacecraft and submarines. NASA
sought to determine the safe levels for long-term exposure to CO2, but found little research focused
on levels below 10,000 ppm CO2; as such, there was no definitive study available to guide standards
(Cronyn et al. 2012). They set the maximum allowable CO2 concentration limits, for long term (1,000
day) habitation of submarines and spacecraft, at 5000 ppm (James and Macatangay 2009).
International Space Station (ISS) crew members have repeatedly reported symptoms associated with
acute CO2 exposure at levels of 5,000 to 6,600 ppm CO2 (see Table 1). The most commonly reported
symptom was headache; other symptoms reported included lethargy, mental slowness, emotional
irritation, and sleep disruption (Law et al. 2010). For space flight, Cronyn et al. (2012) identified three
potential areas of operational impact of elevated CO2: renal calculi (kidney calcification) and bone
reabsorption; cerebral blood flow; and mission performance. With no definitive research to provide
insight into these areas, further evaluation was recommended to examine the effects on human
subjects of various low-to-moderate CO2 concentrations (from ambient levels up to 1%).
Consequently flight rules have been employed to reduce CO2 limits in the ISS to about 3 mm Hg
(4,000 ppm) (Ryder et al. 2017).
6.2 Submarines
Studies of CO2 effects on humans in enclosed submarines have been reviewed by the US government
(Halperin 2007) although most of these studies are for high (> 1%) CO2 levels at relatively short
exposure durations. At these levels (>1%), many of the debilitating and acute symptoms described
above were noted. Current safe levels for continuous exposure in submarines were deemed to be
around 5,000 ppm CO2. This level is set arbitrarily at one-third of the level where there were obvious
signs of health problems (James and Macatangay 2009). It was also noted that if problems are
observed, a submarine can surface so that its occupants can be exposed to the ambient atmosphere.
Halperin (2007) reports that exposures to CO2 levels as low as 7,000 ppm can lower blood pH by up
to 0.05 units and induce renal (kidney) compensation in healthy subjects. This compensation occurs
over a variable period of time, but effects of lowered pH on clinical status or performance have not
been reported either experimentally or operationally. Given that kidney compensation cannot occur
indefinitely, there is some doubt about whether submariners could sustain the “safe” level of 5,000
ppm CO2 if they spent years exposed to it.
7. Protein malfunctions caused by elevated CO2 in the body
Carbon dioxide is a fundamental physiological gas known to profoundly influence the behaviour and
health of millions of species within the plant and animal kingdoms (Phelan et al 2021). It is known
that CO2 plays a major role in sensing and signalling on a cellular level although the physiological
response is complex and not well understood. Research has found that increases in CO2 resulting in
reduced pH alters mitochondrial metabolism reducing oxygen consumption and releasing
intracellular calcium stores (Phelan et al 2021).
The endoplasmic reticulum (ER) is a large dynamic structure within cells that serves many roles
including protein synthesis and calcium storage. Elevated CO2 levels cause protein malfunctions by
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altering ER folding machinery. These malfunctions are associated with ER stress triggering
maladaptive responses and effecting all kinds of diseases e.g., chronic lung disease and reduced
immunity, tissue and organ malfunction (Kryvenko and Vadasz 2021)
7.1 Elevated CO2 causes carbonic anhydrase enzyme disfunction and related diseases
Carbonic anhydrase (CA) enzymes are widely expressed in the nervous system and tissues
throughout the body where they play important physiological roles (Aspatwar et al 2021). The
reaction that CA catalyses, the reversible hydration of CO2 to bicarbonate and a proton, lies at the
heart of a wide range of vital physiological processes (Chegwidden and Carter 2021; Aspatwar et al
2021). Abnormal regulation of carbonic anhydrase-related proteins causes a range of diseases
conditions including cancer, Alzheimer’s, cardiovascular disease, diabetes, glaucoma, epilepsy,
stroke, bipolar disorder etc. The use of CA isozyme inhibitor drugs for treating these diseases is now
a major science (Celebioglu et al 2021; Lemon et al 2021). However, CA inhibitors can cause CO2
retention and result in cellular malfunctions (Phelan et al 2021). The progressive increase in CA
disfunction due to increasing atmospheric CO2 will result in worsening outcomes for the diseases
mentioned above.
7.2 CO2 induced deposits of calcium in the body
Carbonic anhydrase (CA) enzymes participate in metabolic reactions that convert CO2 and result in
the precipitation of calcium carbonate (Adeva-Andany et al. 2015; Kim et al. 2012; Tan et al. 2018).
CA is implicated in calcification of human tissues, including bone and soft-tissue calcification (Adeva-
Andany et al. 2015). The enzyme may be also involved in bile and kidney stone formation and
carcinoma-associated micro-calcifications. The molecular mechanisms regulating the development
of calcification in human tissues and arteries are similar to those that regulate physiological
mineralization in bone tissue, being poorly understood (Adeva-Andany et al. 2015). Carbon dioxide
conversion by the CA enzyme provides bicarbonate and hydrogen ions that fuel the uptake of
ionized calcium which is then deposited in the body tissues as calcium carbonate. With elevated CO2
in cells there is increased release of calcium from the ER (Kryvenko and Vadasz 2021).
Kidney calcification is known to occur with longer term exposure to elevated CO2 levels (Rice 2004;
Schaefer et al., 1979a). A similar causal link between the activity of CA enzyme, which is mainly
responsible for the reversible breakdown of CO2, and calcium deposits has also been established for
arteries (Adeva-Andany et al. 2014). As part of a US Navy experimental program in the 1960’s and
1970’s investigating impacts of long-term CO2 exposure, Schaefer et al (1979b) found that, in a study
of guinea pigs in an enclosed environment breathing 5,000 ppm CO2 for 8 weeks, the kidneys started
to calcify along with bone degradation (see Table 1). Schaefer (1982) also indicated that preliminary
experiments had found kidney calcification effects in animal studies for CO2 concentration as low as
2,000 ppm. Although these studies did not identify a mechanism, they established the casual link
between CO2 and kidney calcification. More recent studies have found that tissue calcification is
promoted where CA is overexpressed due to increased CO2 in the body (Song et al 2021; Phelan et al
2021). Increased CA activity is also linked to cancer where the enzyme helps create a hostile, low pH
environment suitable for cancers to flourish in (Hulikova et al. 2014; Logozzi et al. 2019; Di Fiore et
al. 2020).
12
8. Other important physiological CO2 effects on health
8.1 Impaired growth and muscle development
Female mice exposed to 890 ppm CO2 for 3 months from pre-pregnancy showed reduced growth
(Wyrwoll et al 2022) and a range of lung and respiratory impairments including lower lung
compliance (Larcombe et al. 2021). Prolonged exposure to CO2 on behaviour, hormone secretion
and respiratory muscles in young female rats exposed at 700 ppm CO2 during 6 hours per day for 15
days (Martrette et al. 2017) (see Table 1). CO2 exposure, though not continuous, produced
significant disturbances in behaviour and was accompanied by increased plasma levels of
corticosterone, suggesting that prolonged exposure to CO2 was stressful producing anxiety.
Increased corticosterone associated with hyperactivity in mice was also found from long-term
exposure to 890 ppm CO2.
8.2 Increased cerebral blood flow
Cerebral blood flow (CBF) effects from breathing CO2 is a significant issue for humans. As CO2 in the
blood increases, CBF increases to effectively wash out CO2 from brain tissue and helps regulate
central pH (Ainslie and Duffin, 2009). In a 23-day experiment on humans, Sliwka et al. (1998) found
that cerebral blood flow is increased in the presence of 7,000 ppm (0.7%) CO2 by as much as 35%
(see Table 1) and that CBF remained elevated until the end of the evaluation period, 2 weeks after
the exposure. The impacts of persistent increase in CBF are unclear although there may be a risk of
raised intracranial pressure (ICP) which can compress and damage delicate brain tissue. There is also
evidence that the CBF response to increased CO2 is impaired in Alzheimer’s patients and that this is
linked to the decline in cognitive abilities (Glodzik et al 2013) which will worsen as CO2 in the
atmosphere increases.
8.3 Oxidative Stress
In humans, carbon dioxide is also known to play a role in oxidative stress caused by reactive oxygen
species (ROS) (Ezraty et al. 2011; Kiray et al. 2014). ROS are produced by aerobic metabolism of
molecular oxygen and play a major role in various clinical conditions including malignant diseases,
diabetes, atherosclerosis, chronic inflammation and neurological disorders such as Parkinson’s and
Alzheimer’s diseases (Waris and Ahsan 2006). In particular, oxidative damage to cellular DNA can
lead to mutations resulting in the initiation and progression of cancer. Ezraty et al (2011)
demonstrated that current atmospheric CO2 levels play a role in oxidative stress and that increasing
CO2 levels between 400 and 1,000 ppm exacerbated oxidative stress and damage to DNA in bacteria.
Kiray et al. (2014) concluded that oxidative stress and oxidative damage to brain tissue in mice is
associated with low Insulin-like Growth Factor 1 (IGF-1) levels in mice impacting the growth of bones
and tissues. Increased CO2 promotes the production of ROS leading to greater incidence of cancers
and other diseases including the promotion of virus activity (Waris and Ahsan 2006). Ezraty et et al
(2011) concluded that with higher atmospheric CO2 concentrations, this exacerbation might be of
great ecological concern with important implications for life on Earth.
13
8.4 Inflammation
Inflammation is a serious illness that is known to be caused by elevated CO2 exposure in humans and
animals (Thom et al. 2018; Beheshti et al. 2018; Zappulla 2008; Jacobson et al. 2019). CO2 increases
result in higher levels of Interleukin, a protein involved in regulating immune responses, which
causes inflammation and vascular damage in mice (Thom et al. 2017). Rodents exposed to 3,000
ppm CO2 in spacecraft experiments for 9-13 days showed evidence of inflammation and
physiological stress (Beheshti et al. 2018).
8.5 Stroke
Another study has shown that increased CO2 in the blood of patients can increase the severity of
Subarachnoid haemorrhage; a life-threatening form of stroke, due to the dilatation of arterial
cerebral vessels (Reiff et al 2020).
9. Discussion
Evidence reviewed in this paper suggests that there is a direct risk to the human species posed by
the breathing of ambient atmospheric CO2 concentrations that are rapidly increasing. The level of
ambient atmospheric CO2 that provides unacceptable risk and the exact effect on physiology are not
clearly determined. If this level is reached in the near future, the global human society should be
concerned. Some climate models suggest that atmospheric CO2 levels could be as high as 1,000 ppm
in this century. This is completely unknown for the whole primate evolutionary lineage which has
only experienced levels well below and recently up to the current level of around 410 ppm.
Given the seriousness of the risks identified in this paper an important question has to be: why has
there been no societal discussion of this issue uniquely or in relation to climate change? With the
startling rapid rise of CO2; the permanent changing of our breathable air composition, one would
surely expect the question of whether we can physiologically deal with future projected levels of
CO2, to at least be examined. However, it appears that the issue is not even thought of. There is an
assumption even among scientists that if this was a real issue it would have already been
researched, i.e., we would know about it, though this perception is not scientific and precludes novel
investigation. It appears that the issue of long-term CO2 elevated toxicity has never been significantly
investigated since we have never been in this situation before. Our body’s CO2 compensation
system, as discussed earlier, has been perfectly adequate to deal with a stable level of atmospheric
CO2. It is also possible that climate change has become the main focus of rising CO2 levels and there
is a lack of vested interest amongst climate scientists about the potential dangers of long-term
exposure to elevated CO2. The most recent IPCC report on the health impacts of climate change
didn’t discuss the issue at all (IPCC 2022). This is surprising since the previous IPCC report (Smith and
Woodward 2014) described the findings of Satich et al. (2012) as a reported “reduction in mental
performance at 1,000 ppm CO2 and above, within the range that all of humanity would experience in
some extreme climate scenarios by 2100”. Since the earlier report there have been many more
studies of cognitive decline (Du et al. 2020) and the damaging effects of elevated CO2 on physiology
(this paper). It is therefore disturbing and shocking that the latest IPCC report failed to recognise this
serious and fundamental aspect of climate change. CO2 toxicity at elevated levels is a discipline of
14
environmental medicine which has not focussed on the potential problem because chronic impacts
of increasing environmental CO2 have not yet been recognised. This may also help to explain why
there are very few researchers involved at this stage and public awareness is close to non-existent.
There are few long-term physiological studies of human exposure to 1,000 -2,000 ppm CO2
or less.
However, there are short-term exposure studies describing disease symptoms and physiological
effects as well as reduced cognitive ability in humans at levels around 800 - 950 ppm CO2; these are
CO2 levels that are typically present in offices, classrooms and apartments (Gall et al. 2016). It
appears that many of the physiological effects of CO2 are due to the stimulation of the autonomic
nervous system resulting in elevated blood pressure, respiration, and heart rate (MacNaughton et al.
2016) and this is also associated with a decline in cognitive ability due to increased Cerebral Blood
Flow (CBF) with resulting effects on central nervous system and brain cortical function (Satish et al
2012; Glodzik et al 2013; Bright et al. 2020). The effect on cortical function is supported by a study of
infants that showed an inverse relationship between blood CO2 and electrocortical activity (Wikstrom
et al. 2011). Long-term exposure to environmentally relevant levels of CO2 leads to increases in the
levels of CO2 in human blood (Zheutlin et al. 2014; Hughson et al. 2016; Vehviläinen et al. 2016). This
is retention of CO2 in the human body at greater than normal levels and disturbingly the levels of
CO2 in our blood will continue to increase as atmospheric levels rise.
Increased CO2 in the blood also affects protein behaviour causing inflammation (Thom et al. 2018),
calcification (Schaefer 1982) of body tissue and a range of demonstrated pH-related protein
malfunctions (Duarte et al. 2020), both with potentially serious outcomes. Reduced pH due to CO2
has been found to alter mitochondrial metabolism affecting oxygen consumption (Phelan et al.
2021). Elevated CO2 causing protein malfunctions can trigger diseases including cancer, neurological
disorders, lung disease, reduced immunity and organ failure (Duarte et al 2020; Kryvenko and
Vadász 2021). Perhaps the most significant protein malfunction is the overexpression of the CA
enzyme due to increased CO2 in the body. This widely distributed enzyme plays a vital role allowing
for respiration and the processing of CO2 in all animals and plants. New research is showing that CA
malfunction due to elevated CO2 causes a range of health problems including cancer and diabetes
(Aspatwar et al 2021). Perhaps the most serious of these is tissue calcification which can result in
kidney and cardiovascular failure. Furthermore, the incidence and prevalence of human kidney
calcification (i.e. stones) is increasing globally (Romero et al. 2010; Turney et al. 2011;
Kittanamongkolchai et al. 2018) and it is possible that rising indoor CO2 levels (boosted by increasing
ambient CO2) is the contributing cause.
So what level of permanent CO2 will cause significant calcification and other protein malfunction
effects? It has been suggested that blood pH would be reduced to dangerous levels, if there were no
physiological compensation, at CO2 levels as low as about 430 ppm (Robertson 2006) implying that
ongoing compensation would occur at this level. Ambient conditions may already be dangerously
close to CO2 levels that cause human tissue calcification, particularly when considering the additive
effect of increased ambient levels on indoor CO2 concentrations. In the final paper of the US Navy
CO2 research program in the 1960’s and 1970’s, Schaefer (1982) indicated that this issue had
“become the concern of the Department of Energy and other US government agencies” although it
appears to have been largely forgotten since. If allowed to persist, problems such as kidney and
artery calcification could lead to cardiovascular failure. In the extreme case, lifespans could become
15
shorter than the time required to reach reproductive age. Calcification of kidneys and arteries can be
fatal through renal and cardiovascular failure. This could threaten the viability of human and animal
species without interventions such as the creation of artificial living environments.
Cognitive decline due to CO2, evidenced by definitive studies (Satish et al 2012; Allen et al 2016;
Allen et al 2018) of indoor environments, would logically produce lower intelligence scores in IQ
tests. In fact this phenomenon of declining intelligence is now being measured around the world
(Bratsberg and Rogeberg 2018) with the data suggesting an unidentified environmental cause. It is
feasible that rising outdoor CO2 levels are the cause of the measured decline in human intelligence
(Bierwirth 2018). It is possible that such effects occur without recognition in daily life (Satish et al.
2012). The modest reductions in multiple aspects of decision making, seen as low as 950 ppm (Allen
et al. 2016), may not be critical to individuals, but at a societal level or for employers an exposure
that reduces performance even slightly could be economically significant. The impacts on students
including sickness, reduced attendance and reduced learning abilities should also be a concern for
society. Moreover, the relatively high levels of CO2 in vehicles associated with declining
concentration and fatigue has serious implications for the safety of drivers and their passengers. This
is an issue that does not appear to have been raised in research on driver fatigue illustrating the
general lack of awareness about CO2 effects.
The human species is already impaired in indoor environments and this is likely to get worse as rising
outdoor levels of CO2 contribute to increased indoor concentrations (Azuma et al. 2018). It is not
only humans that are at risk. It has been demonstrated that animals have varying degrees of
susceptibility to carbon dioxide (Schaefer et al. 1971). The impacts of elevated CO2 are even greater
for water breathing animals than air breathing animals. In general, land animals have much higher
blood CO2 than aquatic animals and can compensate for hypercapnia by increasing ventilation. In
aquatic animals, compensation by increased ventilation is rare and a small increase in ambient CO2
causes hypercapnic acidosis (Portner et al. 2004; Knoll et al. 1996; McNeil and Sasse 2016). Studies
have shown that hypercapnia in fish produces substantial neurological, behavioural and
physiological effects (Ishimatsu et al. 2005; Heuer and Grosell 2014) for even short-term exposures
at a CO2 concentration predicted to be persistent in the ocean before the year 2100; this level
corresponding with an atmospheric concentration of 650 ppm CO2 (McNeil and Sasse 2016).
Most of the problems associated with elevated indoor CO2 levels greater than about 800 ppm, can
be alleviated by spending time in fresh air. The indoor environments can be restored to acceptable
CO2 levels with effective ventilation although this is often not being achieved. The available resource
of fresh air may be the underlying misguided reason why there is a lack of concern for pollution and
its effects. Significantly this resource may not be available in the future as rising atmospheric CO2
associated with climate change could exceed the 800 ppm level in the current century (Smith and
Woodward, 2014). At that stage, there would be no outdoor escape from the described symptoms.
Under such a condition of permanent exposure, there could be health impacts at levels less than 800
ppm.
10. Conclusions
16
There is now a significant body of research work that demonstrate (1) current health impacts of
rising CO2 levels and (2) more serious CO2 health impacts for humans at some time in the near
future.
Current impacts of elevated and increasing ambient CO2 in indoor environments include
inflammation, respiratory diseases, headaches, fatigue, increased heart rate, increased blood
pressure, and other symptoms at levels above about 800 ppm. This finding together with the
associated impairment of cognitive abilities at CO2 levels just above ambient (between 600 and 950
ppm) is significant in that it has implications at a societal level for human function particularly for
jobs with critical responsibility (e.g., surgery, air-traffic controllers, drivers etc.) together with the
impact on learning, human development and economies. Physiological CO2 effects will be increased
and more permanent in a future with elevated outdoor ambient CO2 concentrations. Ongoing
impacts may include the exacerbation by CO2 of cellular oxidative stress and protein malfunctions
resulting in an increase in cancers, neurological diseases, viruses and many other conditions. Studies
of health effects at higher levels of CO2 at around 2,000-5,000 ppm demonstrate the impact of the
inability of the body to fully compensate for increased CO2 and acidity in the blood. These effects
include human tissue calcification and bone degradation; the former, associated with the
overexpression of the enzyme carbonic anhydrase that is responsible for processing CO2, might
represent the greatest existential threat for many animals. Given there is a lack of studies in humans
at lower but elevated CO2 levels, demonstrated effects in animals and symptoms experienced by
humans indicate that longer-term mechanisms compensating for increased blood CO2 are active
when breathing at around 800-1000 ppm CO2. Long-term exposure to these and potentially lower
levels would likely cause severe illness. These levels are predicted for the ambient atmosphere by
the end of the century in a “business as usual” world. At some stage in the near future humans could
be experiencing persistent physiological effects resulting in serious health problems.
The risk from rising CO2 levels for human and animal population health in the near-future is
extremely high with the health or survival of species under threat. Communication and global
awareness of this issue alongside climate change would further strengthen the need to drastically
reduce CO2 emissions. New research on the health effects of long-term exposure to realistic future
atmospheric CO2 levels is urgently needed to quantify this risk.
11. References
Abolhassani M, Guais A, Chaumet-Riffaud P, Sasco A, Schwartz L. 2009. Carbon dioxide inhalation causes
pulmonary inflammation. Am J Physiol Lung Cell Mol Physiol 296: L657–L665.
Adeva-Andany MM, Carneiro-Freire N, Donapetry-García C, Rañal-Muíño E, and López-Pereiro Y. 2014. The
Importance of the Ionic Product for Water to Understand the Physiology of the Acid-Base Balance in
Humans. BioMed Research International 2014: Article ID 695281, 16 p. https://doi.org/10.1155/2014/695281.
Adeva-Andany MM, Fernandez-Fernandez C, Sanchez-Bello R, Donapetry-García C, Martínez-Rodríguez J. 2015.
The role of carbonic anhydrase in the pathogenesis of vascular
calcification in humans. Atherosclerosis 241: 183-191.
17
Ainslie PN, Duffin J. 2009. Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing:
mechanisms of regulation, measurement, and interpretation. Am J Physiol Regul Integr Comp Physiol 296:
R1473–1495.
Allen JG, MacNaughton P, Satish U, Santanam S, Vallarino J, Spengler JD. 2016. Associations of Cognitive
Function Scores with Carbon Dioxide, Ventilation, and Volatite Organic Compound Exposures in Office Workers:
A Controlled Exposure Study of Green and Conventional Office Environments. Environmental Health
Perspectives 124: 805.
Allen JG, MacNaughton P, Cedeno-Laurent JG, Cao X, Flanigan S, Vallarino J, Rueda F, Donnelly-McLay D,
Spengler JD. 2018. Airplane pilot flight performance on 21 maneuvers in a flight simulator under varying
carbon dioxide concentrations. Journal of Exposure Science and Environmental Epidemiology · August, DOI:
10.1038/s41370-018-0055-8.
Antic NA. 2012. Global warming and increased sleep disordered breathing mortality, rising carbon dioxide
levels are a serial pest. Respirology 17: 885–886.
Arlot-Bonnemains Y, Fouchereau-Peron M, Moukhar MS, Benson AA, Milhaud G. 1985. Calcium-regulating
hormones modulate carbonic anhydrase II in the human erythrocyte. Proc. Nati. Acad. Sci. USA 82: 8832-8834.
Aspatwar A, Peltola J, Parkkila S. 2021. Targeting Carbonic Anhydrase Isozymes in the Treatment of
Neurological Disorders. In: The Carbonic Anhydrases: Current and Emerging Therapeutic Targets, (Chegwidden
WR, Carter ND Ed). Springer.
Azuma K, Kagi N, Yanagi U, Osawa H. 2018. Effects of low-level inhalation exposure to carbon dioxide in indoor
environments: A short review on human health and psychomotor performance. Environment International
121: 51–56.
Bakó-Biró Z, Clements-Croome DJ, Kochhar N, Awbi HB, Williams MJ. 2011. Ventilation rates in schools and
pupils’ performance. Building and Environment 48: 1-9.
Beheshti A, Cekanaviciute E, Smith DJ, Costes SV. 2018. Global transcriptomic analysis suggests carbon dioxide
as an environmental stressor in spaceflight: a systems biology GeneLab case study. Scientific Reports 8: 4191.
Bierwirth PN. 2018. Are increasing atmospheric carbon dioxide levels lowering our intelligence? ResearchGate
DOI.
Branco PTBS, Alvim-Ferraz MCM, Martins FG, Sousa SIV. 2015. Children's exposure to indoor air in urban
nurseries-part I: CO2 and comfort assessment. Environmental Research 140: 1–9.
Bright MG, Whittaker JR, Driver ID, Murphy K. 2020. Vascular physiology drives functional brain networks.
NeuroImage 217: 116907
Brillante R, Laks L, Cossa G, Peters M, Liu P. 2012. An overnight increase in CO2 predicts mortality in
sleep disordered breathing. Respirology 17: 933-939.
Bruhwiler PA, Stämpfli R, Huber R, Camenzind M. 2005. CO2 and O2 concentrations in integral motorcycle
helmets. Appl Ergon 36(5): 625-633.
Burton RF. 1978. Intracellular buffering. Respiration Physiology 33: 51-58.
18
Campbell AJ, Bolton DPG, Williams SM, Taylor BJ. 1996. A potential danger of bedclothes covering the face.
Acta Paediatr 85(3): 281-284.
Carbon Dioxide Information Analysis Center. 2014. U.S. Department of Energy. Available:
http://cdiac.esd.ornl.gov [accessed 23 December 2014].
Carreiro-Martins P, Viegas J, Papoila AL, Aelenei D, Caires I, Araújo-Martins J, Gaspar-Marques J, Cano
MM, Mendes AS, Virella D, Rosado-Pinto J, Leiria-Pinto P, Annesi-Maesano I, Neuparth N. 2014. CO(2)
concentration in day care centres is related to wheezing in attending children. Eur J Pediatr 173: 1041-1049.
Celebioglu HU, Erden Y, Hamurcu F, Taslimi P, Şentürk OS, Özmen ÜÖ, Tuzun B, Gulçin I. 2021. Cytotoxic
effects, carbonic anhydrase isoenzymes, α-glycosidase and acetylcholinesterase inhibitory properties, and
molecular docking studies of heteroatom-containing sulfonyl hydrazone derivatives. Journal of Biomolecular
Structure and Dynamics 39:15, 5539-5550.
Chegwidden WR, Carter ND. 2021. The Carbonic Anhydrases: Current and Emerging Therapeutic Targets –
Preface, (Chegwidden WR, Carter ND Ed). Springer Nature, Switzerland.
Chiu CF, Chen MH, Chang FH. 2015. Carbon Dioxide Concentrations and Temperatures within Tour Buses under
Real-Time Traffic Conditions. PLoS One 10(4): e0125117.
Colasanti A, Salamon E, Schruers K, van Diest R, van Duinen M, Griez E, 2008. Carbon Dioxide-Induced Emotion
and Respiratory Symptoms in Healthy Volunteers. Neuropsychopharmacology 33: 3103-3110.
Coley DA, Greeves R, Saxby BK. 2007. The effect of low ventilation rates on the cognitive function of a primary
school class. International Journal of Ventilation 6: 107-112.
Constantin D, Mazilescu C, Nagi M, Draghici A, Mihartescu A. 2016. Perception of Cabin Air Quality among
Drivers and Passengers. Sustainability 8: 852; doi:10.3390.
Cronyn PD, Watkins S, Alexander DJ. 2012. Chronic Exposure to Moderately Elevated CO2 during Long-Duration
Space Flight. NASA Technical Report NASA/TP-2012-217358. Available:
http://ston.jsc.nasa.gov/collections/trs/_techrep/TP-2012-217358.pdf [accessed 23 December 2014].
Cui Y, Schubert BA, Jahren AH. 2020. A 23 m.y. record of low atmospheric CO2. Geology 48: 888–892. Available:
https://doi.org/10.1130/G47681.1
Dijken FV, Bronswijk JV, Sundell J. 2005. Indoor environment in Dutch primary schools and health of the pupils.
Proceedings of Indoor Air, Beijing, Vol 1: 623-627.
Di Fiore A, Supuran CT, Scaloni A, De Simone G. 2020. Human carbonic anhydrases and post-translational
modifications: a hidden world possibly affecting protein properties and functions, Journal of Enzyme Inhibition
and Medicinal Chemistry 35(1): 1450-1461.
Du B, Tandoc MC, Mack ML, Siegel JA. 2020. Indoor CO2 concentrations and cognitive function: A critical
Review. Indoor Air 30:1067–1082.
Duarte CM, Jaremko L, Jaremko M. 2020. Hypothesis: Potentially Systemic Impacts of Elevated CO2 on the
19
Human Proteome and Health. Frontiers in Public Health 8: Article 543322.
Eckenhoff RG, Longnecker DE. 1995. The therapeutic gases. Effects of carbon dioxide. In: Goodman and
Gilman’s The Pharmacological Basis of Therapeutics, 9th Ed (Hardman JG,ed). McGraw Hill, 355-356.
Eggleton T. 2013. A short introduction to climate change. Cambridge University Press.
Ezraty B, Chabalier M, Ducret A, Maisonneuve E, Dukan S. 2011. CO2 exacerbates oxygen toxicity. EMBO
Reports 12: 321–326.
Ferrari M, Lodola L, Dellavalle C, Rotondo P, Ricciardi L, Menghini A. 2005. Indoor air quality in an Italian
military submarine. G Ital Med Lav Ergon 27(3): 308-311.
Ferreira AM, Cardoso M. 2014. Indoor air quality and health in schools. J Bras Pneumol 40(3): 259-268.
Gaihre S, Semple S, Miller J, Fielding S, Turner S. 2014. Classroom carbon dioxide concentration, school
attendance, and educational attainment. J Sch Health 84(9): 569-574.
Gall ET, Cheung T, Luhung I, Schiavon S, Nazaroff WW.2016. Real-time monitoring of personal exposures to
carbon dioxide. Building and Environment 104: 59-67.
Gładyszewska-Fiedoruk K.2011. Concentrations of carbon dioxide in the cabin of a small passenger car.
Transportation Research Part D 16: 327–331.
Gładyszewska-Fiedoruk K.2012. Indoor air quality in the cabin of an airliner. Journal of Air Transport
Management 20: 28-30.
Glodzik L, Randall C, Rusinek H, de Leon MJ. 2013. Cerebrovascular reactivity to carbon dioxide in Alzheimer’s
disease. A review. J Alzheimers Dis. 35(3):427-440
Goromosov MS. 1968. The Physiological Basis of Health Standards for Dwellings. World Health Organization
Geneva. Available: http://apps.who.int/iris/handle/10665/39749 [accessed 26 August 2014].
Guais A, Brand G, Jacquot L, Karrer M, Dukan S, Grevillot G, Jo Molina T, Bonte J, Regnier M, Schwartz L. 2011
Toxicity of Carbon Dioxide: A Review. Chem Res Toxicol 24 2061-2070.
Halperin WE. 2007. National Emergency and Continuous Exposure Guidance Levels for Selected Submarine
Contaminants. Vol. 1. National Research Council of the National academies. National Academies Press.
Available: http://www.nap.edu [accessed 9 April 2015].
Henderson R. 2006. Carbon dioxide measures up as a real hazard. Occupational Health & Safety 75.7 : 64,68-
69.
Heudorf U, Neitzert V, Spark J. 2009. Particulate matter and carbon dioxide in classrooms – The impact of
cleaning and ventilation. Int. J. Hyg. Environ. Health 212: 45–55.
Heuer RM. Grosell M. 2014. Physiological impacts of elevated carbon dioxide and ocean acidification on fish.
Am. J. Physiol. Regul. Integr. Comp. Physiol. 307: R1061–R1084.
20
Hughson RL, Yee NJ, Greaves K. 2016. Elevated end-tidal Pco2 during long-duration spaceflight. Aerosp. Med.
Hum. Perform. 87: 894–897.
Hulikova A, Aveyard N, Harris AL, Vaughan-Jones RD, Swietach P. 2014. Intracellular Carbonic Anhydrase
Activity Sensitizes Cancer Cell pH Signaling to Dynamic Changes in CO2 Partial
Pressure. The journal of Biological Chemistry 289 (37): 25418-25430.
IPCC. 2022. Climate Change 2022: Impacts, Adaptation, and Vulnerability. Contribution of Working Group II to
the Sixth Assessment Report of the Intergovernmental Panel on Climate Change [H.-O. Pörtner, D.C. Roberts,
M. Tignor, E.S. Poloczanska, K. Mintenbeck, A. Alegría, M. Craig, S. Langsdorf, S. Löschke, V. Möller, A. Okem, B.
Rama (eds.)]. Cambridge University Press. Cambridge University Press, Cambridge, UK and New York, NY, USA,
3056 pp.
Ishimasu A, Hayashi M, Lee KS, Kikkawa T, Kita J. 2005. Physiological effects on fishes in a high-CO2 world. J.
Geophys. Res. 110: C09S09, doi:10.1029/2004JC002564.
Jacobson TA, Kler JS, Hernke MT, Braun RK, Meyer KC, Funk WE. 2019. Direct human health risks of increased
atmospheric carbon dioxide. Nature Sust. 2: 691-701.
James JT, Macatangay A. 2009. Carbon Dioxide – Our Common “Enemy” . NASA Technical report JSC-CN-
18669. SAMAP Submarine Air Monitoring Air Purification Conference, 19-22 October 2009, San Diego, CA.
Available: http://ntrs.nasa.gov/archive/nasa/casi.ntrs.nasa.gov/20090029352.pdf [accessed 9 April 2015].
Jurado SR, Bankoff ADP, Sanchez A. 2014. Indoor air quality in Brazilian universities. International journal of
environmental research and public health 11(7): 7081-7093.
Kajtar L, Herczeg, L. 2012. Influence of carbon-dioxide concentration on human well-being and intensity of
mental work. Q. J. Hung. Meteorol. Serv 116: 145–169.
Karnauskas KB, Miller SL, Schapiro AC. 2020. Fossil fuel combustion is driving indoor CO2 toward levels harmful
to human cognition. GeoHealth 4, e2019GH000237. https://doi.org/ 10.1029/2019GH000237.
Kim IG, Jo BH, Kang DG, Kim CS, Choi YS, Cha HJ. 2012. Biomineralization-based conversion of carbon dioxide to
calcium carbonate using recombinant carbonic anhydrase. Chemosphere 87: 1091-1096.
Kiray, M, Sisman AR, Camsari UM, Evren, Day A, Baykara B, Aksu I, Ates M, Uysalet N. 2014. Effects of carbon
dioxide exposure on early brain development in rats. Biotech Histochem. 89: 371-383.
Kittanamongkolchai W, Vaughan LE, Enders FT, Dhondup T, Mehta RA, Krambeck AE, McCollough CH, Vrtiska
TJ, Lieske JC, Rule AR. 2018. The changing incidence and presentation of urinary stones Over 3 Decades. Mayo
Clin Proc. 93: 291-299.
Knoll AH, Bambach RK, Canfield DE, Grotzinger JP. 1996. Comparative Earth History and Late Permian Mass
Extinction. Science 273: 452-457.
Kryvenko V, Vadász I. 2021. Mechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction.
Frontiers in Physiology 12.
Kukadia V, Ajiboye P, White M. 2005. Ventilation and indoor air quality in schools, BRE Information paper
IP06/05. Watford: BRE publication.
21
Law J, Watkins S, Alexander, D. 2010. In-Flight Carbon Dioxide Exposures and Related Symptoms: Associations,
Susceptibility and Operational Implications. NASA Report TP–2010–216126. Available:
http://ston.jsc.nasa.gov/collections/trs/_techrep/TP-2010-216126.pdf [accessed 26 August 2014].
Larcombe AN, Papini MG, Chivers EK, Berry LJ, Lucas RM, Wyrwoll CS. 2021. Mouse Lung Structure and
Function after Long-Term Exposure to an Atmospheric Carbon Dioxide Level Predicted by Climate Change
Modeling. Environmental Health Perspectives 129(1): https://doi.org/10.1289/EHP7305.
Lee SC, Chang M. 2000. Indoor and outdoor air quality investigation at schools in Hong Kong. Chemosphere
41(1-2): 109-113.
Lemon N, Canepa E, Ilies MA, Fossati S. 2021. Carbonic Anhydrases as Potential Targets Against Neurovascular
Unit Dysfunction in Alzheimer’s Disease and Stroke. Frontiers in Aging Neuroscience 16 (13) 772278.
Logozzi M, Capasso C, Di Raimoa R, Del Prete S, Mizzoni D, Falchi M, Supuran CT, Faisa S. 2019. Prostate cancer
cells and exosomes in acidic condition show increased carbonic anhydrase IX expression and activity. Journal of
Enzyme Inhibition and Medicinal Chemistry 34 (1): 272-278.
Lu CY, Lin JM, Chen YY, Chen YC. 2015. Building-related symptoms among office employees associated with
indoor carbon dioxide and total volatile organic compounds. International journal of environmental research
and public health 12(6): 5833-5845.
MacNaughton P, Spengler, Vallarino J, Santanam S, Satish U, Allen J. 2016. Environmental perceptions and
health before and after relocation to a green building. Building and Environment 104: 138-144.
Mardones ML, Thatje S, Fenberg PB, Hauton C. 2022. The short and long-term implications of warming
and increased sea water pCO2 on the physiological response of a temperate neogastropod species. Marine
Biology 169 (1): 3.
Martrette JM, Egloff C, Clément C, Yasukawa K, Thornton SN, Trabalon M. 2017. Effects of prolonged exposure
to CO2 on behaviour, hormone secretion and respiratory muscles in young female rats. Physiology & Behavior
177: 257–262.
McNeil B, Sasse T. 2016. Future ocean hypercapnia driven by anthropogenic amplification of the natural CO2
cycle. Nature 529: 383-386.
Muscatiello N, McCarthy, A, Kielb C, Hsu WH, Hwang SA, Lin S. 2015. Classroom conditions and CO2
concentrations and teacher health symptom reporting in 10 New York State Schools. Indoor Air 25(2): 157-167.
National Institute for Occupational Safety and Health (NIOSH). 1996. Criteria for a Recommended Standard,
Occupational Exposure to Carbon Dioxide. August 1976. In: Documentation for Immediately Dangerous to Life
or Health Concentrations (IDLHs) for carbon dioxide. Available: www.cdc.gov/niosh/docs/1970/76-194.html
[accessed 23 December 2014].
Navarro JM, Andrade-Villagran´ PV, Manríquez PH, Duarte C, Chaparro OR. 2022. Long-term effects of
contrasting pCO2 levels on the scope for growth in the carnivorous gastropod Concholepas concholepas.
Marine Environmental Research 175: 105586.
22
OSHA (Occupational Safety and Health Administration). 2012. Sampling and Analytical Methods: Carbon
Dioxide in Workplace Atmospheres. Available: http://www.osha.gov/dts/sltc/methods/ino
rganic/id172/id172.html [accessed 23 December 2014].
Pang L, Zhang J, Cao X, Wang X, Liang J, Zhang L, Guo L. 2020. The effects of carbon dioxide exposure
concentrations on human vigilance and sentiment in an enclosed workplace environment
Indoor Air 31:467–479.
Patton KT, Thibodeau GA. 2009. Anatomy & Physiology. 7th ed. St Louis. Mosby.
Phelan DE, Mota C, Lai C, Kierans SJ, Cummins EP. 2021. Carbon dioxide-dependent signal transduction in
mammalian systems. Interface Focus 11(2):20200033.
Portner HO, Langenbuch M, Reipschlager A. 2004. Biological Impact of Elevated Ocean CO2 Concentrations:
Lessons from Animal Physiology and Earth History. Journal of Oceanography 60:705-718.
Raven P, Johnson G, Mason K, Losos J, Singer S. 2007. Biology. 8th ed. New York. McGraw-Hill.
Reiff T, Barthel O, Schönenberger S, Mundiyanapurath S. 2020. High-normal PaCO2 values might be
associated with worse outcome in patients with subarachnoid hemorrhage – a retrospective cohort study.
BMC Neurology 20:31. https://doi.org/10.1186/s12883-020-1603-0.
Rice SA. 2004. Human health risk assessment of CO2: Survivors of acute high-level exposure and populations
sensitive to prolonged low-level exposure. Third Annual Conference on Carbon Sequestration. 3-6 May 2004,
Alexandria, Virginia, USA. Available: http://www.netl.doe.gov/publications/proceedings/04/carbon-
seq/169.pdf [accessed 13 April 2015].
Robertson DS. 2006. Health effects of increase in concentration of carbon dioxide in the atmosphere. Current
Science 90:1607-1609.
Romero V, Akpinar P, Assimos DG. 2010. Kidney Stones: A Global Picture of Prevalence, Incidence, and
Associated Risk Factors. Reviews in Urolology 12: e86–e96.
Ryder V, Scully R, Alexander D, Lam C, Young M, Satish U, Basner M. 2017. Effects of acute exposures to carbon
dioxide upon cognitive functions. In: Proceedings of NASA Human Research Program Investigators’ Workshop.
(23–26 Jan 2017. Galveston, TX). Washington, DC.
Santamouris M, Synnefa A, Asssimakopoulos M, Livada I, Pavlou K, Papaglastra M, Gaitani N, Kolokotsa D,
Assimakopoulos V. 2008. Experimental investigation of the air flow and indoor carbon dioxide concentration in
classrooms with intermittent natural ventilation. Energy and Buildings 40; 1833–1843.
Satish U, Mendell MJ, Shekhar K, Hotchi T, Sullivan D, Streufert S, Fisk WJ. 2012. Is CO2 an Indoor Pollutant?
Direct Effects of Low-to-Moderate CO2 Concentrations on Human Decision-Making Performance.
Environmental Health Perspectives 120:1671-1677.
Schaefer KE, Hastings BJ, Carey CR, Nichols JR. 1963. Respiratory acclimatization to carbon dioxide. Journal of
Applied Physiology 18:1071-1078.
23
Schaefer KE, Niemoller H, Messier A, Heyder E, Spencer J. 1971. Chronic CO2 Toxicity: Species Difference in
Physiological and Histopathological Effects. Report No 656, pp 1_26, US Navy Dept, Bureau of Medicine and
Surgery, Naval Submarine Medical Center, Submarine Medical Research Laboratory, Groton, CT.
Schaefer KE, Pasquale SM, Messier AA, Niemoeller H. 1979a. CO2-Induced Kidney Calcification. Undersea
Biomed Res. Suppl 6:S143-S153.
Schaefer KE, Douglas WHJ, Messier AA, Shea ML, Gohman PA. 1979b. Effect of Prolonged Exposure to 0.5%
CO2 on Kidney Calcification and Ultrastructure of Lungs. Undersea Biomed Res. Suppl 6:S155-S161.
Schaefer K E. 1982. Effects of increased ambient CO2 levels on human and animal health. Experientia 38:1163-
1168.
Schmidt S. 2020. CO2 is trending: See the latest atmospheric concentrations data on Twitter. CSIROscope 28
February, https://blog.csiro.au/co2-data-twitter/
Scripps Institution of Oceanography. 2020. A daily record of global atmospheric carbon dioxide concentration.
UC San Diego. https://scripps.ucsd.edu/programs/keelingcurve/
Scott JL, Kraemer DG, Keller RJ. 2009. Occupational hazards of carbon dioxide exposure. Journal of Chem
Health and Safety 16:18-22.
Scully RR, Basner M, Nasrini J, Lam C, Hermosillo E, Gur RC, Moore T, Alexander DJ, Satish U, Ryder VE. 2019.
Effects of acute exposures to carbon dioxide on decision making and cognition in astronaut-like subjects. NPJ
Microgravity 5: 17.
Seppänen OA, Fisk WJ, Mendell MJ. 1999. Association of Ventilation Rates and CO2-Concentrations with
Health and other Responses in Commercial and Institutional Buildings. Indoor Air 9: 226-252.
Shriram S, Ramamurthy K, Ramakrishnan S. 2019. Effect of occupant-induced indoor CO2 concentration and
bioeffluents on human physiology using a spirometric test. Building and Environment 149: 58–67.
Sliwka U, Krasney JA, Simon SG, Schmidt P, Noth J. 1998. Effects of sustained low-level elevations of carbon
dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. Aviat Space Environ
Med 69:299-306.
Smith KR, Woodward A. 2014. Chapter 11. Human health: impacts, adaptation, and co-benefits. In: IPCC, 2014:
Climate Change 2014: Impacts, Adaptation, and Vulnerability. Part A: Global and Sectoral Aspects. New York,
709-754. Available: http://ipcc-wg2.gov/AR5/report/full-report/ [accessed 26 August 2014].
Snow S, Boyson A, King M, Malik O, Coutts L, Noakes C, Gough H, Barlow J, Schraefel M. 2018. Using EEG to
characterise drowsiness during short duration exposure to elevated indoor Carbon Dioxide
concentrations https://t.co/HaJ0UZRADx #bioRxiv. doi: https://doi.org/10.1101/483750.
Snow S, Boyson AS, Paas KHW, Gough H, King M, Barlow J, Noakes CJ, Schraefel MC. 2019. Exploring the
physiological, neurophysiological and cognitive performance effects of elevated carbon dioxide concentrations
indoors. Building and Environment 156: 243–252.
Song X, Li P, Li Y, Yan X, Yuan L, Zhao C, An Y, Chang X. 2021. Strong association of glaucoma with
atherosclerosis. Scientific Reports 11: 8792.
24
Stolp H. 2022. Developing in a polluted atmosphere: A link between long-term exposure to elevated
atmospheric CO2 and hyperactivity. Journal of Physiology 600(6): 1275-1276.
Tan S, Han Y, Yua Y, Chiu C, Chang Y, Ouyang S, Fan K, Lo K, Nga I. 2018. Efficient carbon dioxide sequestration
by using recombinant carbonic anhydrase. Process Biochemistry 73: 38-46.
Thom SR, Bhopale VM, Hu J, Yang M. 2017. Inflammatory responses to acute elevations of carbon dioxide in
mice. J Appl Physiol 123: 297-302.
Tsai DH, Lin JS, Chan CC. 2012. Office workers' sick building syndrome and indoor carbon dioxide
concentrations. J Occup Environ Hyg 9(5): 345-351.
Tu Z, Li Y, Geng S, Zhou K, Wang R, Dong X. 2020. Human responses to high levels of carbon dioxide and air
temperature. Indoor Air 00:1–15.
Turney BW, Reynard JM, Noble JG, Keoghane SR. 2011. Trends in urological stone disease. BJU International
109: 1082-1087.
Vehviläinen T, Lindholm H, Rintamäki H, Pääkkönen R, Hirvonen A, Niemi O, Vinha J. 2016. High indoor CO2
concentrations in an office environment increases the transcutaneous CO2 level and sleepiness during
cognitive work. J. Occupational and Environmental Hygiene 13: 19-29.
Waris G, Ahsan H. 2006 Reactive oxygen species: role in the development of cancer and various chronic
conditions. Journal of Carcinogenesis 5: 14.
Widory D, Javoy M. 2003. The carbon isotope composition of atmospheric CO2 in Paris. Earth and Planetary
Science Letters 215: 289-298.
Wikstrom S, Lundin F, Ley D, Pupp IH, Fellman V, Rosén I, Hellström-Westaset L. 2011. Carbon dioxide and
glucose affect electrocortical background in extremely preterm infants. Pediatrics 127(4): e1028-1034.
Wyrwoll CS, Papini MG, Chivers EK, Yuan J, Pavlos NJ, Lucas RM, Bierwirth PN, Larcombe AN. 2022. Long-term
exposure of mice to 890 ppm atmospheric CO2 alters growth trajectories and elicits hyperactive behaviours in
young adulthood. Journal of Physiology 600(6): 1439-1453.
Xia Y, Shikii S, Shimomura Y. 2020. Determining how different levels of indoor carbon dioxide affect human
monotonous task performance and their effects on human activation states using a lab experiment: a tracking
task. Ergonomics, DOI:10.1080/00140139.2020.1784466 Available:
https://doi.org/10.1080/00140139.2020.1784466
Xu X, Lian Z, Shen J, Cao T, Zhu J, Lin X, Qing K, Zhang W, Zhang T. 2020. Experimental study on sleep quality
affected by carbon dioxide concentration. Indoor Air 31:440–453.
Yang Y, Sun C, Sun M. 1997. The effect of moderately increased CO2 concentration on perception of coherent
motion. Aviat Space Environ Med 68: 187-91.
Zachos J, Pagani M, Sloan S, Thomas E, Billups K. 2001. Trends, rhythms, and aberrations in global climate 65
Ma to present. Science; 292, 5517.
25
Zappulla D. 2008. Environmental stress, erythrocyte dysfunctions, inflammation, and the metabolic syndrome:
adaptations to CO2 increases? J. Cardiometab. Syndr. 3: 30–34.
Zhang J, Pang L, Cao X, Wanyan X, Wang X, Liang J, Zhang L. 2020. The effects of elevated carbon dioxide
concentration and mental workload on task performance in an enclosed environmental chamber. Building and
Environment 178: 106938.
Zhang X, Wargocki P, Lian Z, Thyregod C. 2017. Effects of exposure to carbon dioxide and bioeffluents on
perceivedair quality, self-assessed acute health symptoms, and cognitive performance. Indoor Air 27: 47-63.
Zheutlin AR, Adar SD, Kyun Park S. 2014. Carbon dioxide emissions and change in prevalence of obesity and
diabetes in the United States: an ecological study. Environment International: 73, 111–116.
... Έτσι εξηγείται η συνεχής συσσώρευσή του στην ατμόσφαιρα και η καθοριστική του συμβολή στην υπερθέρμανση του πλανήτη (φαινόμενο του θερμοκηπίου) που προκαλεί την κλιματική κρίση και δημιουργεί εύλογες ανησυχίες για τη δυνατότητά μας να επιβιώσουμε στον πλανήτη (Bierwirth 2021 Οι πρωτοφανείς αυτές καταγραφές του CO2 13 είναι πολύ σημαντικές γιατί μας δίνουν μια ένδειξη του σε ποιο επίπεδο θα πρέπει να θεωρείται ότι είναι η συγκέντρωση του CO2 στην εξωτερική ατμόσφαιρα, αφού η τιμή του CO2 εξωτερικά θεωρείται από πολλά πρότυπα η βάση υπολογισμού του επιθυμητού επιπέδου του CO2 στους εσωτερικούς χώρους. Για παράδειγμα υπάρχει διαδεδομένη η άποψη ότι οι οδηγίες του ASHRAE (ASHRAE 2016) προτείνουν +700 ppm CO2 από την τιμή του CO2 στην εξωτερική ατμόσφαιρα, για την οποία δέχονται το, ξεπερασμένο από καιρό, επίπεδο των 300 ppm CO2, δηλαδή 1000 ppm CO2 (300+700=1000 ppm) ως το ανώτατο επιθυμητό όριο για το CO2 στους εσωτερικούς χώρους (Persily 2020). ...
... Αναλυτικότερα, η υπερκαπνία, όπως ονομάζεται η αυξημένη συγκέντρωση CO2 στο αίμα, συνήθως εμφανίζεται ως αποτέλεσμα υποαερισμού, δηλαδή, όταν δεν φτάνει επαρκές οξυγόνο στους πνεύμονες, επειδή το σώμα είτε δεν λαμβάνει επαρκές φρέσκο οξυγόνο ή δεν απομακρύνει κατάλληλα το CO2 (Bierwirth 2021). Σε περίπτωση που η υπερκαπνία δεν αποτελεί σύμπτωμα υποκειμένων παθήσεων, που επηρεάζουν την αναπνοή και το αίμα, τότε μπορεί να οφείλεται σε μολυσμένο με διοξείδιο του άνθρακα αέρα που αναπνέει κανείς (Wikipedia 2021b). ...
... Τα έντονα συμπτώματα της υπερκαπνίας (ανεξήγητο αίσθημα σύγχυσης, μη φυσιολογικό συναίσθημα παράνοιας ή κατάθλιψης, μυϊκοί σπασμοί, ανώμαλος καρδιακός ρυθμός, κρίσεις πανικού, επιληπτικές κρίσεις, λιποθυμία) θέτουν το ανθρώπινο σώμα σε πραγματική απειλή, γιατί μπορεί να αποτρέψουν τη φυσιολογική αναπνοή 17 (Bierwirth 2021). ...
Thesis
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Η μελέτη αυτή παρουσιάζει μια εξαμηνιαία έρευνα (από Ιανουάριο έως Ιούνιο του 2019) αναφορικά με τα επίπεδα συγκέντρωσης του διοξειδίου του άνθρακα (CO2) σε τάξεις ενός δημοτικού σχολείου. Το CO2 είναι ένα βασικό ανθρωπογενές αέριο ρύπανσης, που συνδέεται στενά με την ποιότητα του εσωτερικού αέρα (Indoor Air Quality/IAQ), που, με τη σειρά του, είναι ένας σημαντικός παράγοντας της εσωτερικής περιβαλλοντικής ποιότητας (Indoor Environ mental Quality/IEQ). Τα υψηλά επίπεδα CO2 έχουν αποδειχθεί ότι επηρεάζουν σημαντικά τη συνολική ποιότητα του εσωτερικού αέρα (IAQ), επηρεάζοντας την υγεία και τη γνωστική λειτουργία, οδηγώντας σε πολλές απουσίες από τα σχολεία (ή την εργασία), σε προβλήματα υγείας και σε μειωμένα ακαδημαϊκά (ή παραγωγικά) αποτελέσματα. Δεδομένου ότι τα ελληνικά σχολεία, στην πλειονότητά τους, δεν έχουν τεχνητά συστήματα μόνιμου εξαερισμού στα κτίριά τους, όπως και το σχολείο της μελέτης, η έρευνα προσπάθησε να διαπιστώσει εάν ο φυσικός αερισμός (παράθυρα) και ο βοηθητικός αερισμός (ανεμιστήρες) είναι αρκετά για να διατηρήσουν τα επίπεδα του CO2 σε αποδεκτά επίπεδα, όπως καθορίζουν τα πρότυπα ασφαλείας (<1000 ppm). Ένας αισθητήρας (Kane Alert CO2) τοποθετούνταν εναλλακτικά σε δυο αίθουσες διδασκαλίας και κάθε 10 λεπτά καταγραφόταν το επίπεδο του CO2 σε ppm (καθώς και η θερμοκρασία δωματίου σε C) κατά τη διάρκεια των μαθημάτων της τάξης. Ο βαθμός συσσώρευσης του CO2 στην τάξη αξιολογήθηκε σε σχέση με τη θερμοκρασία δωματίου, το μέγεθος της τάξης, το ύψος της τάξης, τον αριθμό των μαθητών, τον αριθμό των ανοιχτών παραθύρων, το μέγεθος των παραθύρων, το αν η πόρτα της αίθουσας ήταν ανοικτή ή όχι, το μέγεθος της πόρτας, και συνδυάστηκε με εξωτερικά μετεωρολογικά δεδομένα (θερμοκρασία, ταχύτητα ανέμου, βροχή, ατμοσφαιρική πίεση) που ανακτήθηκαν από το Εθνικό Αστεροσκοπείο Αθηνών (Μετεωρολογικός Σταθμό Περιστερίου, που απέχει 1,8 χλμ. από το σχολείο) . Το επίπεδο του CO2 που συσσωρεύεται στις σχολικές τάξεις κατά τη διάρκεια των μαθημάτων αποτελεί ένα ισχυρό δείκτη για την επίτευξη καλής σχολικής, γνωστικής και μαθησιακής, επίδοσης και η γνώση του γεγονότος αυτού μπορεί να οδηγήσει σε αλλαγές συμπεριφοράς (συνεχής συνειδητοποίηση των επιπέδων IAQ, άνοιγμα παραθύρων κ.λπ.) που θα εξασφαλίζουν τα αποδεκτά επίπεδα CO2 μέσα στη σχολική αίθουσα και, συνεπακόλουθα, θα εξασφαλίζουν καλύτερα ακαδημαϊκά αποτελέσματα για τους μαθητές των σχολείων μας. This is a presentation of a six- month period survey (from January to June 2019) on the Carbon Dioxide (CO2) levels in 2 primary school’s classrooms. CO2 is a basic anthropogenic pollutant gas, closely associated with Indoor Air Quality (IAQ) and a major factor in Indoor Environmental Quality (IEQ). Higher levels of CO2 have been proved to lower significantly the overall IAQ, affecting health and cognitive function, leading to many absences from schools (or work), to health problems and deteriorating academic (or work production) results. Given the fact that Greek schools, in their vast majority, lack any artificial permanent ventilation systems in their buildings, such as the school in consideration, the survey tried to establish whether natural ventilation (windows) and assisted ventilation (fans) was enough to keep the CO2 levels within accepted standards (<1000 ppm). A sensor was placed in two classrooms (Kane Alert CO2) and the CO2 level (in ppm) plus room temperature (in C) was recorded every 10 mins during class lessons. The rate of CO2 accumulation in the classroom was evaluated in reference with room temperature, classroom size, classroom elevation, students’ number, number of open windows, size of windows, whether door was open or not, size of door, whether radiators (cold period) or fans (warm period) were working and general official meteorological data (temperature, wind speed, air pressure, rain) retrieved from National Observatory of Athens (Peristeri meteorological station, which is situated just 1,8 km away from the case school). Knowing the CO2 levels in school classrooms during lessons is a strong indicator of the resultant school cognitive and learning productivity and can lead to behavioural changes (constant awareness for “feeling” IAQ levels, opening of windows, etc.) that can keep CO2 levels within accepted standards and thus secure better academic results for schools and their students.
... • Exposure to CO2 levels is another factor affecting IAQ and occupants' comfort levels and should be considered (Bierwirth, 2021). ...
Thesis
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In existing school buildings in Quebec, natural ventilation is often the only solution for thermal comfort and indoor air quality control. However, many studies show insufficiently ventilated classrooms, leading to indoor environment quality problems. Where the arbitrary use of natural ventilation can lead to energy overconsumption, several studies have been conducted on the role of natural ventilation on this issue, but few of them are addressed in very cold climates. This research investigates the impact of natural ventilation on thermal comfort, indoor air quality, and energy efficiency of school buildings in cold climates. Various architectural parameters associated with windows were analyzed for a typical classroom in the Schola.ca corpus. Since most of these school buildings are not equipped with HVAC systems and have only infrastructures for conventional heating systems, the lack of indoor air quality is an inevitable problem. In this research, the windows' orientation, position, opening size, and opening position, natural ventilation program, and window-opening modes (single-sided and cross-window openings) were numerically simulated with the Ladybug Tools software. The software outputs consist of annual numerical data (temperature, humidity, mean radiant temperature, CO2 concentration, energy, and thermal) representing thermal comfort and IAQ performances in school buildings and their impacts on energy consumption efficiency. In analyzing the result, several standards and guidelines were used, including ASHRAE 55 standard models (Predicted Mean Vote PMV and Adaptive Thermal Comfort models ATC for thermal performance), the Health Canada and National Collaboration Centre for Environmental Health guideline, and the Federation of European Heating, Ventilation and Air Conditioning Associations REHVA to evaluate the building thermal and IAQ performances compared to the recommended benchmark models. The results show that repetitive short-term opening of the windows could be an optimal solution in terms of thermal comfort, indoor air quality, and heating energy consumption efficiency. Natural ventilation solutions could retrieve the lack of indoor air quality and the cost of HVAC system renovation; however, they should be only applied during cold seasons to avoid thermal discomfort and energy overconsumption.
... 41 Furthermore, ailments such as headaches, hearing loss, sweating and fatigue, rapid pulse rate, and blood acidosis had been associated with exposure to high level of CO 2 . 42 The health problems associated with CH 4 are slurred speech, memory loss, nausea, mood changes, vision problems, facial flushing, vomiting, and headache. 43 ...
Article
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This study assessed the air quality, health status and lung function of workers from intensive poultry production systems in selected areas of Ogun State. Air samples were monitored monthly between November 2017 and April 2018 from six pens in three selected poultry zones of Ogun state. The air pollutants (CO2, CH4, NO2, NH3, H2S, SO2, PM2.5) and the microclimatic parameters around the poultry pens were determined. Copies of structured questionnaires were administered to assess the impacts of air pollutants on the health status of the poultry workers. Lung function parameters namely: Forced Expiratory Volume in 1 s (FEV1), Forced Vital Capacity (FVC), FEV1/FVC and Peak Expiratory Flow Rate (PEFR) were measured to assess the pulmonary health of the poultry workers and the control group. The levels of NH3, PM2.5, CO2 and CH4 were higher than the permissible standards while NO2, H2S and SO2 were below the permissible limits of the World Health Organization. Regression analysis between pollutants and microclimatic parameters showed that relative humidity and windspeed had negative effects on PM2.5, NO2, H2S and SO2. FEV1/FVC measured for poultry workers was 86.84 ± 18.32% with 10.0% having obstructive lung function, while the control group had 98.82 ± 1.52% with 100% normal lung function pattern. The predicted PEFR for poultry workers was significantly lower at 61.12 ± 27.85% with 13.3% having severe airway restrictions, while the predicted PEFR for the control group was significantly higher at 88.41 ± 21.76% with no severe airway narrowing. This study established that air quality around the poultry operations affected the workers’ health.
... In addition to the problems of global warming caused by the high percentage of carbon dioxide in the atmosphere, it affects humans and in the long term, with the emergence of many health problems. These include chronic infections, kidney failure, bone atrophy, loss of brain function, as well as an increased incidence of cancer [23]. ...
Conference Paper
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This paper aims to demonstrate the importance of natural gas as a substantial source of energy as an alternative to crude oil, with the increase in global demand for it in the future, and the importance of this source for Iraq at the economic and environmental level. This article provides an overview of Iraq's natural gas reserves and the geographical distribution of this reserve over the regions of Iraq, in addition to the companies operating and developers there. The challenges facing the export and industry of gas in Iraq, the quantities of gas that are flared annually, and the associated financial and environmental damage were also presented. Finally, if the quantities of produced gas were to be invested, Iraq would achieve a significant improvement in the economic and environmental levels.
... Zheutlin et al. (2014) also proved an indication of a link between CO 2 and obesity. This potential health damage lasts long, affecting the body's absorption of certain essential elements (Bierwirth, 2018;Weyant et al., 2018). See Fig. 1 for details. ...
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Excessive greenhouse gas emissions might be the major culprit for environmental degradation, which have direct and indirect adverse impacts in various ways. As the largest emitter of carbon emissions, China suffered great harm from climate change during the past 40 years. Therefore, it becomes necessary to study the impact of carbon emissions on health issues and their potential mechanism. Using the panel data from 30 provinces in China between 2002 and 2017, this study employes and extends the Stochastic Impacts by Regression on Population, Affluence, and Technology (STIRPAT) model and mediating effect model to analyze the direct and indirect effects of carbon emissions. The main results are as follows: (1) Carbon emissions has a certain negative impact on public health, which would increase with the rise of temperature. (2) The increase in carbon emissions has a more significant negative effect on health with the average temperature exceeding 17.75 °C, indicating that the temperature has a threshold effect. (3) The potential health risks become higher with the development of urbanization, but there is no obvious spillover effect in the health consequences. The results remain robust after controlling other factors. This study supplements the literature of climate governance and human health, potentially contributing to the next stage of high-quality and sustainable development.
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LOCKDOWN PHASE OF COVID 19 AND ENVIRONMENTAL RESPONSE.pdf
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References consulted for writing this book CHAPTER 1: INTRODUCTION TO COVID-19 Today the whole world is under the appalling shadow of COVID pandemics. The disease has posed severe adverse impacts on almost all sectors of the society encompassing health, education, recreation, food, transportation and economic profile. However, the environmental sector is noted for its improvement due to complete closures of transport systems, industries, tourisms and even pilgrims. The chapter has thrown light on the status of the pandemics in terms of infection and mortality, the common symptoms of the disease and sketched an overview of the adverse impacts of COVID- 19 on different sectors, except environment. The annexure at the end of the chapter focuses on an innovative alternative livelihood befitted for the COVID and post- COVID situations. Keywords COVID- 19. Symptoms of COVID. Social Distancing. Vaccine. Mask References 1. Biscayart C, Angeleri P, Lloveras S, Chaves T, Schlagenhauf P, Rodriguez-Morales AJ (2020) The next big threat to global health? 2019 novel coronavirus (2019-nCoV): What advice can we give to travellers? Interim recommendations January2020, from the Latin-American Society for Travel Medicine (SLAMVI). Travel MedInfect Dis 101567. doi:10.1016/j.tmaid.2020.101567 2. Carlos WG, DelaCruz CS, Cao B, Pasnick S, Jamil S (2020) Novel Wuhan (2019-nCoV) coronavirus. Am J Respir Crit Care Med 201: 7-8 3. Chen N, Zhou M, Dong X, Qu J, Gong F, Han Y, et al. (2020) Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptivestudy. Lancet 395:507-513, doi:10.1016/S0140-6736(20)30211-7 4. Gorbalenya AE, Baker SC, Baric RS, deGroot RJ, Drosten C, Gulyaeva AA, et al. (2020) Severe acute respiratory syndrome-related coronavirus: the species and its viruses-a statement of the Coronavirus Study Group. Bio R xiv, doi:10.1101/2020.02.07.937862. 5. Guan W, Ni Z, Hu Yu, Liang W, Ou C, He J, Liu L, Shan H, Lei C, et al. (2019) Clinical Characteristics of Coronavirus Disease 2019 in China. N Engl J Med, 1-13, doi: 10.1056/NEJMoa2002032. 6. Holshue ML, DeBolt C, Lindquist S, Lofy KH, Wiesman J, Bruce H, et al. (2020) First case of 2019 novelcoronavirus in the United States. NEngl J Med, doi:10.1056/NEJMoa2001191. 7. http://www.who.int 8. https://www.oecd.org/berlin/publikationen/Interim-Economic-Assessment-2-March-2020.pdf 9. https://www.expresscomputer.in/news/covid-19/ai-finds-9-potential-coronavirus-covid-19-drugs-that-can-be-used-on-humans-immediately/51446/ 10. https://jansuvidhakendrakatiakammu.blogspot.com/2020/03/indiafightscorona-covid-19.html 11. https://www.marketwatch.com/story/these-nine-companies-are-working-on-coronavirus-treatments-or-vaccines-heres-where-things-stand-2020-03-06. 12. https://www.mayoclinic.org/diseases-conditions/coronavirus/symptoms-causes/syc-20479963 13. https://www.nbcnews.com/health/health-care/here-are-3-drugs-development-fight-coronavirus-2-vaccines-one-n1163191 14. https://www.oecd.org/berlin/publikationen/Interim-Economic-Assessment-2-March-2020.pdf 15. https://www.spglobal.com/en/research-insights/featured/credit-markets-coronavirus 16. https://www.wired.com/story/japan-is-racing-to-test-a-drug-to-treat-covid-19/ 17. https://www.worldometers.info/coronavirus/ 18. https://economictimes.indiatimes.com/industry/healthcare/biotech/healthcare/the-road-to-covid-19-vaccine-much-progress-some- hiccups/articleshow/78456523.cms?utm_source=contentofinterest&utm_medium=text&utm_campaign=cppst 19. Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. (2020) Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 395: 497–506 20. Li Q, Guan X, Wu P, Wang X, Zhou L, Tong Y, et al. (2020) Early transmission dynamics in Wuhan, China, of novel coronavirus-infected pneumonia. N Engl J Med, doi:10.1056/NEJMoa2001316. 21. Li Z, Yi Y, Luo X, et al. (2020) Development and clinical application of a rapid IgM-IgG combined antibody test for SARS-CoV-2 infection diagnosis. J Med Virol https://doi.org/10.1002/jmv.25727 22. Lu H, Stratton CW, Tang YW (2020) Outbreak of pneumonia of unknown etiology in Wuhan China: the mystery and the miracle. J Med Virol, doi:10.1002/jmv.25678. 23. Mao L, Wang M, Chen S, He Q, et al. (2020) Neurological Manifestations of Hospitalized Patients with COVID-19 in Wuhan, China: A Retrospective Case Series Study (https://ssrn.com/abstract=3544840 or http://dx.doi.org/10.2139/ssrn.3544840) 24. McGee P (2006) Natural Products re-emerge. Drug Dis Dev, 9:18-26. 25. Wang C, Horby PW, Hayden FG, Gao GF (2020) A novel coronavirus outbreak of global health concern. Lancet 395: 470-473 26. World Health Organization; 2020 (WHO/2019-nCoV/NDVP/2020.1). Licence: CC BY-NC-SA 3.0 IGO. Guidance on developing a national deployment and vaccination plan for COVID-19 vaccines. Geneva: 27. Young BE, Ong SWX, Kalimuddin S, Low JG, Tan SY, Loh J, et al. (2020) Epidemiologic Features and Clinical Course of Patients Infected With SARS-CoV-2 in Singapore. JAMA, doi: 10.1001/jama.2020.3204. 28. Zhao S, Lin Q, Ran J, Musa SS, Yang G, Wang W, et al. (2020) Preliminary estimation of the basic reproduction number of novel coronavirus (2019-nCoV) in China, from 2019 to 2020: a data-driven analysis in the early phase of the outbreak. Int J Infect Dis 92: 214-217 CHAPTER 2: IMPACT OF COVID-19 LOCKDOWN ON AIR QUALITY Pure air is a mixture of several gasses with nitrogen constituting the highest proportion followed by oxygen, argon, carbon dioxide etc. During the lockdown phase of COVID- 19 the air quality has been found to be much better than non-COVID periods. Due to complete closures of the industries, transport sectors, recreational units, offices and business houses, the carbon dioxide level of the mega city of Kolkata (India) showed a significant dip, which has been explained in this chapter in details. Even in the mangrove dominated Indian Sundarbans the same trend is observed when the data of pre-COVID and COVID lockdown phases were compared. Keywords Air quality. COVID- 19 lockdown. Kolkata. Atmospheric CO2. Indian Sundarbans References 1. Agarwal S, Banerjee K, Pal N, Mallik K, Bal G, Pramanick P, Mitra A (2017b) Carbon sequestration by mangrove vegetations: A case study from Mahanadi mangrove wetland. J Env Sci Comp Sci Eng Tech 7(1):16-29 2. Agarwal S, Pal N, Zaman S, Mitra A (2017a) Role of mangroves in carbon sequestration: A case study from Prentice island of Indian Sundarbans. Int J Basic Appl Res 7(7):35-42 3. Alongi DM (2016) Climate Regulation by Capturing Carbon in Mangroves. The Wetland Book. I: Structure and Function, Management and Methods. Springer Netherlands 1-7 4. Banerjee K, Agarwal S, Pal N, Mitra A (2017) Bhitarkanika Mangrove Forest: A Potential Sink of Carbon. Int J Res Cul Soc 1(7):280-286 5. Banerjee K, Roy Chowdhury M, Sengupta K, Sett S, Mitra A (2012) Influence of anthropogenic and natural factors on the mangrove soil of Indian Sundarbans wetland. Arch Environ Sci 6:80-91 6. Banerjee R, Pramanick P, Zaman S, Pal N, Mitra S, Mitra A (2015) Impact of Urban vegetation on offsetting Carbon emission: A case study from the city of Kolkata. J Env Sci Comp Sci Eng Tech 4(3):814-818 7. Bierwirth PN (2018) Carbon dioxide toxicity and climate change: a major unapprehended risk for human health. Web Published: ResearchGate DOI, 10 8. Chakraborty S, Zaman S, Pramanick P, Raha AK, Mukhopadhyay N, Chakravartty D, Mitra A (2013) Acidification of Sundarbans mangrove estuarine system. Dis Nature (ISSN: 2319-5703) 6(14):14-20 9. Dutta J, Saha A, Mitra A (2016) Impact of acidification on heavy metal levels in a bheri of East KolkataWetlands (EKW), a Ramsar Site in the Indian sub-continent. Int J Adv Res Biol Sci 3(11):154-159 10. Ewel KC, Twilley RR, Ong JE (1998) Different kinds of mangrove forests provide different goods and services. Global Ecol Biogeogr 7:83-94 11. Guha Bakshi BN, Sanyal P, Naskar KR (1998) Sundarban Mangals, Naya Prakash, Kolkata. 12. https://edition.cnn.com/2020/03/31/asia/coronavirus-lockdown-impact-pollution-india-intl-hnk/index.html 13. https://edition.cnn.com/2020/04/02/health/aerosol-coronavirus-spread whitehouseletter/index.html 14. https://timesofindia.indiatimes.com/city/bhopal/Heat-stroke-kills-7-in-Madhya-Pradesh/articleshow/52403498.cms 15. https://www.bbc.com/future/article/20200326-covid-19-the-impact-of-coronavirus-on-the-environment 16. https://www.co2.earth/daily-co2 17. https://www.iqair.com/world-most-polluted-cities 18. https://www.mvweathercenter.com/wxhistory.php?date=201904 19. https://nhess.copernicus.org/preprints/nhess-2017-107/nhess-2017-107.pdf 20. https://www.ucsusa.org/resources/each-countrys-share-co2-emissions 21. https://www.who.int/emergencies/diseases/novel-coronavirus-2019 22. Le DH, Bloom SA, Nguyen QH, Maloney SA, Le QM, Leitmeyer KC, Bach HA, Reynolds MG, Montgomery JM, Comer JA, Horby PW, Plant AJ (2004) Lack of SARS transmission among public hospital workers Vietnam. Emerg Infect Dis 10:265-268 23. Mitra A (2013) Mangroves: A Unique Gift of Nature, in: Sensitivity of Mangrove ecosystem to changing Climate. Springer, New Delhi, India:33-105 24. Mitra A (2019) Estuarine Pollution in the Lower Gangetic Delta, Springer International Publishing, ISBN 978-3-319-93305-4, XVI:371 25. Mitra A, Rudra T, Guha A, Ray A, Pramanick P, Pal N, Zaman S (2016) Ecosystem service of Avicennia alba in terms of Carbon sequestration. J Env Sci Comp Sci Eng Tech 5(1):155-160 26. Mitra A, Sengupta K, Banerjee K (2012) Spatial and temporal trends in biomass and carbon sequestration potential of Sonneratia apetala Buch-Ham in Indian Sundarbans. Proc Nat Aca Sci India Sec B Biol Sci 82(2):317-323 27. Mitra A, Zaman S (2014) Carbon sequestration by Coastal Floral Community, India. The Energy and Resources Institute (TERI) TERI Press. ISBN 978-81-7993-551-4 28. Mitra A, Zaman S (2015) Blue carbon reservoir of the blue planet, Springer, ISBN 978-81 322-2106-7 29. Mitra A, Zaman S (2016) Threats to marine and estuarine ecosystems, in: Basics of Marine and Estuarine Ecology. Springer India:365-417 30. Mitra, A. and Zaman, S (2020) Environmental Science – A ground Zero Observation on the Indian Subcontinent, Springer International Publishing, Switzerland, ISBN 978-3-030- 49130-7 31. Mitra S, Fazli P, Zaman S, Jana HK, Pramanick P, Pal N, Mitra A (2015) Molluscan community: a potential sink of carbon. J Energy Env Carbon Cre 5(3):1-4 32. Naskar KR, Mandal RN (1999) Ecology and Biodiversity of Indian Mangroves, Daya Publishing House New Delhi 33. Pal N, Mitra A, Zaman S, Mitra A (2019) Natural oxygen counters in Indian Sundarbans, the mangrove dominated World Heritage Site. Par J Sci Edu 5(2):6-13 34. Ray Chaudhuri T, Fazli P, Zaman S, Pramanick P, Bose R, Mitra A (2014) Impact of acidification on heavy metals in Hooghly Estuary. J Harm Res Appl Sci 2(2):91-97 35. Robertson DS (2006) Health effects of increase in concentration of carbon dioxide in the atmosphere. Curr Sci 1607-1609 36. Roychowdhury R, Zaman S, Roy M, Mitra, A (2018) Study on the health of Hooghly estuary in terms of coliform load. Techno Int J Health Eng Manag Sci 2:40-47 37. Zaman S, De UK, Pramanick P, Thakur S, Amin G, Fazli P, Mitra A (2014) Forecasting heavy metal level on the basis of acidification trend in the major estuarine system of Indian Sundarbans, J Energy Env Carbon Credit 4(2):1-9 CHAPTER 3: IMPACT OF COVID-19 LOCKDOWN ON MARINE AND ESTUARINE WATER QUALITY The marine and estuarine waters are subject to significant anthropogenic disturbances due to rapid pace of industrialization, urbanization, tourism expansion and shrimp culture proliferation in the Indian sub-continent. The COVID- 19 lockdown phase witnessed a complete reverse picture in the lower Gangetic water profile with the upgradation of water quality in terms of dissolved oxygen (DO), heavy metals and water pH. A detailed study on the alteration of dissolved Zn in coastal West Bengal during COVID- 19 lockdown phase has added value to the chapter especially for interested readers. Keywords Coastal and estuarine water. Dissolved heavy metals. Aquatic pH. Dissolved Oxygen (DO) References 1. Agarwal S, Fazli P, Zaman S, Pramanick P, Mitra A (2019) Seasonal variability of acidification in major estuaries of Indian Sundarbans. Glo J Eng Sci Res, 6(4):493-498 2. Agarwal S, Pramanick P, Mitra A (2020) Alteration of dissolved Zinc concentration during COVID-19 lockdown phase in coastal West Bengal. NUJS J Regul Studies, (Special Edition), 51-56. 3. Al-Masri MS, Aba A, Khalil H, Al-Hares Z (2002) Sedimentation rates and pollution history of a dried lake: Al-Oteibeh Lake. Sci Total Environ 293(1-3):177-189 4. Chakraborti D, Adams F, Van Mol W, Irgolic JK (1987) Determination of trace metals in natura waters at nanogram per litre levels by Electrothermal Atomic Absorption Spectrophotometry after extraction with sodium diethyldithiocarbamate. Anal Chem Acta 196:23-31 5. Chakraborty S, Zaman S, Pramanick P, Raha AK, Mukhopadhyay N, Chakravartty D, Mitra A (2013) Acidification of Sundarbans mangrove estuarine system. Dis Nature 6(14):14-20 6. Dutta J, Saha A, Mitra A (2016) Impact of acidification on heavy metal levels in a bheri of East KolkataWetlands (EKW), a Ramsar Site in the Indian sub-continent. Int J Adv Res Biol Sci 3(11):154-159 7. Duzgoren-Aydin N, Wong C, Song Z, Aydin A, Li X, You M (2006) Fate of heavy metal contamination in road dusts and gully sediments in Guangzhou, SE China: A chemical and mineralogical assessment. Hum Ecol Risk Assess 12:374-389 8. Florea A, Busselberg D (2006) Occurrence, use and potential toxic effects of metals and metal compounds. Biomet 19:419-427 9. Gbem TT, Balogun JK, Lawaland FA, Annune PA (2001). Trace metals accumulation in Clarias gariepinus Teugules exposed to sun lethal levels of tannery effluent. Sci Total Environ 271:1-9 10. Holland HD (1978) The Chemistry of the Atmosphere and Oceans. Wiley, New York, 351 11. Jadeja BA, Odedra NK, Thaker MR (2006) Studies on ground water quality of industrial area of Dharampur, Porbandar city, Saurashtra, Gujrat, India. Plant Arch 6(1):341-344 12. Keenan CP, Davie P, Mann D (1998) A revision of the genus Scylla De Haan, 1833 (Crustacea: Decapoda: Brachyura: Portunidae). Raff Bull Zool 46:217-245 13. Khare S, Singh S (2002) Histopathological lesions by copper sulphate and lead nitrate in the gills of fresh water fish Nandus. J Ecotoxicol Environ Mont 12:105-111 14. Knauer GA. (1977). Immediate industrial effects on sediment metals in a clean coastal environment. Mar Poll Bull 8:249-254 15. Mitra A (2000) The Northeast coast of the Bay of Bengal and deltaic Sundarbans. In: Seas at the Millennium – An environmental evaluation, Chapter 62 (Editor: Charles Sheppard, University of Warwick, Coventry, UK), Elsevier Sci 143-157 16. Mitra A (2013) In: Sensitivity of Mangrove Ecosystem to Changing Climate. Publisher Springer New Delhi Heidelberg New York Dordrecht London, 2013 edition; ISBN-10: 8132215087; ISBN-13: 978-8132215080 17. Mitra A (2019) Estuarine Pollution in the Lower Gangetic Delta. Published by Springer International Publishing, ISBN 978-3-319-93305-4, XVI:371 18. Mitra A, Banerjee K, Ghosh R, Ray SK (2010) Bioaccumulation pattern of heavy metals in the shrimps of the lower stretch of the River Ganga. Mesopot J Mar Sci 25(2):1-14 19. Mitra A, Bhattacharyya DP (2003) Environmental issues of shrimp farming in mangrove ecosystem. J Ind Ocean Stud 11(1):120-129 20. Mitra A, Ray Chadhuri T, Mitra A, Pramanick P, Zaman S (2020) Impact of COVID-19 related shutdown on atmospheric carbon dioxide level in the city of Kolkata. P J Sci Edu 6(3):84-92. 21. Mitra A, Zaman S (2014) Carbon sequestration by Coastal Floral Community, India. Published by The Energy and Resources Institute (TERI) TERI Press. ISBN 978-81-7993-551-4 22. Mitra A, Zaman S (2016) Basics of Marine and Estuarine Ecology Published by Springer, ISBN 978-81-322-2705-2 23. Pytkowicz RM, Kester DR (1971) The Physical Chemistry of Seawater. Oceanogr Mar Biol Ann Rev 9:11-60 24. Ray Chaudhuri T, Fazli P, Zaman S, Pramanick P, Bose R, Mitra A (2014) Impact of acidification on heavy metals in Hooghly Estuary. J Harm Res Appl Sci 2(2):91-97 25. Roychowdhury R, Vyas P, Zaman S, Roy A, Mitra A (2019) Surface water pH: A proxy to acidification of estuarine water of Indian Sundarbans. Int J Res Anal Rev 6(1):1530-1535 26. Satish RS (2011) Indian Estuaries: Dynamics, ecosystems and threats; Natl Acad Sci Lett 34(7 & 8) 27. Stoffers P, Glasby GP, Wilson CJ, Davis KR, Walter P (1986) Heavy metal pollution in Wellington Harbour. New Zealand J Mar Fresh Water Res 20:495-512 28. Turekian, KK (1968) Oceans. Published by Prentice Hall, ISBN-10: 0136303684; ISBN-13: 978-0136303688, 120 29. Zaman S, De UK, Pramanick P, Thakur S, Amin G, Fazli P, Mitra A (2014) Forecasting heavy metal level on the basis of acidification trend in the major estuarine system of Indian Sundarbans. J Energ Environ Carbon Cred 4(2):1-9 Internet Reference www.nltr.org CHAPTER 4: IMPACT OF COVID-19 LOCKDOWN ON COASTAL BIODIVERSITY The lower Gangetic delta sustaining the mangrove dominated Indian Sundarbans is known for rich taxonomic diversity. The deltaic complex is presently under threat due to unplanned urbanization, tourism, fishing and release of industrial wastes almost without treatment. This causes a negative impact on the biotic community structure of the region. During COVID- 19 lockdown phase, the situation changed almost radically due to overall paralysis of almost all the anthropogenic activities. This strict lockdown restored the biodiversity spectrum in terms of ichthyoplankton and also decreased the coliform load in the water body. The chapter explains this restoration process with Ground- Zero data. Keywords Indian Sundarbans. Biodiversity. Ichthyoplankton. Total Coliform. Phytoplankton References 1. Annandale A (1907) The fauna of the brackish ponds at Port Canning, Lower Bengal. Rec. Indian Museum 1:33-43 2. APHA (1998) Standard Methods for the Examination of Water and Wastewater. 20th edition. American Public Health Association, Washington, DC 3. Banerjee K, Mitra A, Bhattacharyya DP, Choudhury A (2000) A preliminary study of phytoplankton diversity and water quality around Haldia port-cum-industrial complex. Proceedings of the National Seminar on "Protection of the Environment - An urgent need" 15-18 4. Boto KG, Wellington JT (1984) Soil Characteristics and Nutrient Status in a Northern Australian Mangrove Forest. Estuaries 7(1):61-69. 5. Brett MT, Goldman CR (1996) A meta-analysis of the freshwater trophic cascade Proc Natl Acad Sci USA 93:7723–7726. 6. Brett MT, Goldman CR (1997) Consumer versus resource control in freshwater pelagic food webs Sci 275:384–386. 7. Carmichael WW (1994) The toxins of cyanobacteria Sci Ame Jan 78–102 8. Carpenter SR, Kitchell JF, Hodgson JR (1985) Cascading trophic interactions and lake productivity BioSci 35:634–639 9. Chaudhuri AB, Choudhury A (1994) In: Mangroves of the Sundarbans. Volume I: India. Published by IUCN- The World Conservation Union 10. Clark LD, Hannon NJ (1967) The mangrove swamp and salt marsh communities of the Sydney district. I. Vegetation, soils, and climate. J Ecol 55:753-771 11. Coppejans E, Beeckman H, De Wit M (1992) The seagrass and associated macroalgal vegetation of Gazi Bay (Kenya). Hydrobiol 247:59-75 12. Costa CSB, Davy AJ (1992) Coastal salt marsh communities of Latin America. In: Seeliger, U. (Ed.), Coastal Plant Communities of Latin America. Academic Press, San Diego 179–199 13. De Laune RD, Patrick WH, Bran~O~ JM (1976) Nutrient transformation in Louisiana salt marsh soils. Louisiana State University, Baton Rouge, Louisiana. Sea Grant Publication No LSlT-T-76-009 14. Falconer IR (1999) An overview of problems caused by toxic blue–green algae (cyanobacteria) in drinking and recreational water Environ Toxicol 14:5–12 15. Farnsworth EJ, Ellison AM (1996) Sun-shade adaptability of the Red Mangrove, Rhizophora mangle (Rhizophoraceae): Changes through ontogeny at several levels of biological organization. Am J Botany 83(9):1131-1143 16. Gupta SK (1987) Some mangrove soils of the Sunderbans ecosystem. UNESCO Regional Introductory Training Course on Estuarine Research, Calcutta 1:105-112 17. Hesse PR (1961) The decomposition of organic matter in a mangrove swamp soil. Plant Soil XIV(3) 18. Hora SL (1934) Brackish water animals of Gangetic Delta. Curr Sci 2:426-427 19. Jhingran VG (1982) Fish and Fisheries of India. Hindustan Publication Corporation New Delhi 666 20. Kaliaperumal N (1994) Seaweed Resources of Tamil Nadu Coast. Biology-Education, Oct-Dec 281-293 21. Kangas PC, Lugo AE (1990) The distribution of mangroves and saltmarshes in Florida. Trop Ecol 31:32-39. 22. Kathiresan K, Moorthy P, Rajendran N (1994) Seedling performance of mangrove Rhizophora apiculata (Rhizophorales: Rhizophoraceae) in different environs. Ind J Mar Sci 23(3):168-169. 23. Kemp S (1917) Notes on Fauna of the Matla river in the Gangetic delta. Rec. Indian Mus 13:233-292. 24. Khan RA (2003) Fish faunal resources of Sundarban estuarine system with special reference to the Biology of some commercially important species. Rec Zool Survey Ind, Occasional Paper 209:1-150 25. Koch MS, Snedaker SC (1997) Factors influencing Rhizophora mangle L. seedling development in Everglades carbonate soils. Aquat Bot 59(1‐2):87‐98 26. Lacerda LD (1998) Biogeochemistry of Trace Metals and Diffuse Pollution in Mangrove Ecosystems. International Society for Mangrove Ecosystems, Okinawa, 64 p. [A review on contaminants biogeochemistry, mobility and bioavailability within mangroves and its applicability in pollution control] 27. Lalli CM, Parsons TR (1997) Biological Oceanography: An Introduction, 2nd Edn, 314. Oxford: Butterworth-Heinmann. 28. Lana PDC, Guiss C, Disaro ST (1991) Seasonal variation of biomass and production dynamics for aboveground and belowground components of a Spartina alterniflora marsh in the Euhaline sector of Paranagua Bay (SE Brazil). Estuar Coast Shelf Sci 32(3):231-242 29. Mandal AK, Nandi NC (1989) Fauna of Sundarban Mangrove Ecosystem, West Bengal, India. Fauna of Conservation Areas, Zoological Survey of India 30. Mazda Y, Sato Y, Sawamoto S, Yokochi H, Wolanski E (1990) Links between physical, chemical and biological processes in Bashita-minato, a mangrove swamp in Japan. Estuar Coast Shelf Sci 31(6):817-833 31. McQueen DJ, Post, JR, Mills EL (1986) Trophic relationships in freshwater pelagic ecosystems Can J Fish Auat Sci 43:1571–1581 32. Micheli F (1999) Eutrophication, fisheries, and consumerresource dynamics in marine pelagic ecosystems Sci 285:1396–1398 33. Mitra A (2000) The north-west coast of the Bay of Bengal and deltaic Sundarbans, In: Seas at the Millennium: An Environmental Evaluation, U.K. 2:160 34. Mitra A (2013) In: Sensitivity of Mangrove Ecosystem to Changing Climate. Publisher Springer New Delhi Heidelberg New York Dordrecht London, 2013 edition; ISBN-10: 8132215087; ISBN-13: 978-8132215080 35. Mitra A (2019) Estuarine Pollution in the Lower Gangetic Delta. Published by Springer International Publishing, ISBN 978-3-319-93305-4, XVI:371 36. Mitra A, Gangopadhyay A, Dube A, Andre, Schmidt CK, Banerjee K (2009) Observed changes in water mass properties in the Indian Sundarbans (Northwestern Bay of Bengal) during 1980-2007. Curr Sci 1445-1452 37. Mitra A, Sengupta K, Banerjee K (2011) Standing biomass and carbon storage of above-ground structures in dominant mangrove trees in the Sundarbans. For Ecol Manage 261(7):1325-1335. 38. Mitra A, Zaman S (2014) Carbon sequestration by Coastal Floral Community, India. Published by The Energy and Resources Institute (TERI) TERI Press. ISBN 978-81-7993-551-4 39. Mitra A, Zaman S (2015) Blue carbon reservoir of the blue planet published by Springer ISBN 978-81-322-2106-7 (Springer DOI 10.1007/978-81-322-2107-4) XII pp:299 40. Mitra A, Zaman S (2016) Basics of Marine and Estuarine Ecology; Publisher Springer India, ISBN 978-81-322-2707-6;1-481 41. Motomura S (1962) The Effect of Organic Matter on the Formation of Ferrous Ion in Soil. Soil Sci Plant Nutr 8:20-29 42. Patrick Jr WH, Mikkelsen DS (1971) Plant nutrient behavior in flooded soil. In Fertilizer technology and use, 2nd ed., ed. R. A. Olson, 187–215. Madison, Wisc. Soil Sci Soc Am 43. Pauly D, Christensen, V (1995) Primary production required to sustain global fisheries Nature 374:255– 257 44. Phillips A, Lambert G, Granger JE, Steinke TD (1994) Horizontal zonation of epiphytic algae associated with Avicennia marina (Forssk.) Vierh. Pneumatophores at Beachwood Mangroves Nature Reserve, Durban, South Africa. Bot Mar 37(6):567-576 45. Pillay TVR (Ed.) (1967) FAO Fishery Report, (44), 1(2): 55 p. Proceedings of the FAO World Symposium on Warm-water Pond Fish Culture, Rome, Italy 18–25th May 1966 46. Poovachiranon S, Chansang H (1994) Community structure and biomass of seagrass beds in the Andaman Sea. I. Mangrove-associated seagrass beds. Phu Mar Biol Center Res Bull 59:53–64. 47. Ruttner F (1963) Fundamentals of limnology (Ed). Tr. German, O.G. Frey and F.E.J. Fry, Toronto, Uni. of Toronto, Press. 295 48. Steinke TD, Naidoo Y (1990) Biomass of algae epiphytic on pneumatophores of the mangrove, Avicennia marina, in the St. Lucia Estuary. S Afr J Bot 56:226–232 49. Stolicza F (1869) The malacology of lower Bengal and the adjoining provinces, 1, on the genus Onchidium. J Asiat Soc Bengal 38:86-111 50. Surendran PK, Thampuran N, Nambiar N (2000) Comparative microbial ecology of freshwater and brackishwater prawn farms. Fish Technol 37:25-30 51. Tussenbroek BI van (1995) Thalassia testudinum leaf dynamics in a Mexican Caribbean coral reef lagoon. Mar Biol 122:33-40 52. Vargas CA, Escribano R, Poulet S (2006) Phytoplankton food quality determines time windows for successful zooplankton reproductive pulses Ecol 8:2992-2999 53. Vollenweider RA (1976) Advances in defining critical loading levels for phosphorus in lake eutrophication Memorie dell’Istituto Italiano d’Idrobiologia 33:53-83 CHAPTER 5: IMPACT OF COVID-19 ON LIVELIHOODS OF LOWER GANGETIC DELTA Indian Sundarbans in the lower Gangetic delta with a population of some 4.2 million is facing severe impact as the majority of the existing livelihoods like fishing, wood collection, honey collection, handicraft etc. have been stopped either due to complete closure of vessels and boats during the lockdown period or to comply with the strict rules of social distancing. In the midst of COVID phase, the super cyclone Amphan hit the Gangetic delta on 20th May, 2020 and devastated the livelihood sector of the region. This chapter throws light on few innovative livelihoods befitted to COVID situation that have high probability to upgrade the economic profile of the region. Keywords Indian Sundarbans. Livelihoods. Amphan. Innovative livelihoods References 1. Agarwal S, Zaman S, Biswas S, Pal N, Pramanick P, Mitra A (2016) Spatial variation of mangrove seedling carbon with respect to salinity: A case study with Bruguiera gymnorrhiza seedling. Int J Advanc Res Biol Sci 3(8):7-12 2. Ahmed F, Hossain MY, Fulanda B, Ahmed ZF, Ohtomi J (2012) Indiscriminate exploitation of wild prawn post larvae in the coastal region of Bangladesh, A threat to the fisheries resources, community livelihoods and biodiversity. Ocean Coast Manag 56-62 3. Bandaranayke MW (2002) Bioactivities Bioactive Compounds and Chemical Constituents of Mangrove Plant. Wetl Ecol Manag 10:421-452 4. Banerjee K, Ghosh R, Homechaudhuri S, Mitra A (2009) Seasonal variation in the biochemical composition of red seaweed (Catenella repens) in Indian Sundarbans. J Earth Sys Sci, Springer Verlag 118(5):497-505 5. Chong VC (1980) The biology of the white prawn Penaeus merguiensis de Man (Crustacea: Penaeidae) in the Pulau Angsa Klang Strait waters (Straits of Malacca). M. Sc. thesis. Department of Zoology, University of Malaya, Kuala Lumpur pp. 141 6. Chopin T, Yarish C (1999) Seaweeds must be a significant component of aquaculture for an integrated ecosystem approach. Bull Aquacult Assoc Can 99:35-37 7. Chowdhury GR, Pal N, Zaman S, Saha A, Mitra A (2017) Shrimp Seed Collection in Indian Sundarban Estuaries: A Threat to Overall Estuarine Ecosystem Services. J Environ Soc Sci 4(1):127 8. de Reuver M, Sørensen C, Basole RC (2017) The Digital Platform: A Research Agenda. J Inf Tech 33(2):124–135 9. Essaidi I, Brahmi Z, Snoussi A, Koubaier HBH, Casabianca H, Abe N, Omri AE, Chaabouni MM, Bouzouita N (2013) Phytochemical investigation of Tunisian L. Salicornia herbacea, antioxidant, antimicrobial and cytochrome P450 (CYPs) inhibitory activities of its methanol extract. Food Cont 32:125-133 10. Gawer A, Cusumano MA (2014) Industry platforms and ecosystem innovation. J Prod Innov Manag 31(3):417–433 11. https://www.hindustantimes.com/analysis/covid-19-india-is-staring-at-a-mental-health-crisis/story-hmBOzUYsbo3SmtlWilmBzL.html 12. https://zeenews.india.com/india/sunderban-takes-up-beekeeping-to-stop-tiger-attacks-will-sell-honey-online-2304032.html 13. ICUN (1989) Marine Protected Areas Needs in the South Asian Seas Regions. 2, India. 14. Leh MUC, Sasekumar A (1984) Feeding ecology of prawns in shallow waters adjoining mangrove shores. In: Proceedings of the Asian symposium on mangrove environment – research and management, Kuala Lumpur, pp. 331–353 15. Mandal AB (2002) Prospective Rice cultures for rainfed coastal saline soils of West Bengal. J Ind Soc Coast Agricul Res 20(1):37-40 16. Martínez-Porchas M, Martínez-Córdova LR, Porchas-Cornejo MA, López-Elías JA (2010) Shrimp polyculture: a potentially profitable, sustainable, but uncommon aquacultural practice. Rev Aquac 2:73-8 17. McIntyre DP, Srinivasan A (2017) Networks, platforms, and strategy: Emerging views and next steps. Strat Manag J 38(1):141–160 18. Mitra A (1998) Status of coastal pollution in West Bengal with special reference to heavy metals. J Ind Ocean Stud 5(2):135–138 19. Mitra A (2013) In: Sensitivity of Mangrove Ecosystem to changing Climate. (Springer DOI: 10.1007/978-81-322-1509-7) pp. 323 20. Mitra A, Banerjee K, Samanta S, Jana HK, Basu S (2006) Edible oyster culture in Indian Sundarbans. In: Mitra A, Banerjee K (eds) Training manual on non-classical use of mangrove resources of Indian Sundarbans for alternative livelihood programmes, 1st edn. Unit I, WWF-India, Canning Field Office, West Bengal, pp. 11–28 21. Mitra A, Choudhury A, Zamaddar YA (1992) Effects of heavy metals on benthic molluscan communities in Hooghly estuary. Proc Zool Soc 45:481-496 22. Mitra A, Pal N, Chakraborty A, Mitra A, Saha A, Trivedi S, Zaman S (2016b) Estimation of stored carbon in Sonneratia apetala seedlings collected from Indian Sundarbans. Ind J Geo Mar Sci 45(11):1598-1602 23. Mitra A, Saha A, Pal N, Fazli P, Zaman S (2016a) Allometry in S. apetala seedlings of Indian Sundarbans. Int J Rec Adv Multidiscip Res 3:1903-1909 24. Mitra A, Sundaresan J, Banerjee K, Agarwal SK (2017) In: Environmental coastguards. Published by CSIR-National Institute of Science Communication and Information Resources (CSIR-NISCAIR), ISBN 978-81-7236-352-9 25. Mitra A, Zaman S (2014) Carbon Sequestration by Coastal Floral Community; published by The Energy and Resources Institute (TERI) TERI Press, India, ISBN 978-81-7993-551-4 pp. 300 26. Mitra A, Zaman S (2015) Blue carbon reservoir of the blue planet, published by Springer, ISBN 978-81-322-2106-7 (Springer DOI 10.1007/978-81-322-2107-4) XII pp. 299 27. Mitra A, Zaman S (2016) Basics of Marine and Estuarine Ecology, Springer, ISBN 978-81-322-2705-2 DOI: https://doi.org/10.1007/978-81-322-2707-6 XII pp. 483 28. MPEDA (2021) State-wise aqua culture productivity – MPEDA; http://mpeda.gov.in 29. Niyogi S, Mitra A, Saha SB, Choudhury A (1999) Interrelationship between diversity of prawn juveniles and mangroves in Sager Island, West Bengal, India. Proc Zool Soc Cal 52(2):85-88 30. Pal N, Gahul A, Zaman S, Biswas P, Mitra A (2016) Spatial Variation of Stored Carbon in Avicennia alba Seedlings of Indian Sundarbans. Int J Trend Res Dev 3(4):100-103 31. Parker G, Van Alstyne M, Choudary S (2016) Platform Revolution: How Networked Markets Are Transforming the Economy and How to Make Them Work For You. New York: W.W.Norton 32. Perez Farfante I, Kensley BF (1997) Penaeids and Sergestoid Shrimps and Prawns of the World:Keys and Diagnoses for the Families and Genera. Muséum national d'Histoire naturelle, Paris pp. 233 (Mémoires du Muséum national d'Histoire naturelle; 175) 33. Petrell RJ, Mazhari Tabrisi K, Harrison PJ, Druehl LD (1993) Mathematical model of Laminaria production near a British Columbian salmon sea cage farm. J Appl Phycol 5:1–14 34. Pornpitakdamrong A, Sudjaroen Y (2014) Seablite (Suaeda maritima) product for cooking, Samut Songkram province-Thailand. Food Nutr Sci 5:850-856 35. Roy Chowdhury G, Mitra A (2017) Traditional Halophytic Medicine: A New Era in the Health Care Canvas. Org Med Chem Int J 555584 (DOI: 10.19080/OMCIJ.2017.02.555584) 2(2):1-3 36. Santhanam R, Ramanathan N, Jegatheesan G (1990) Coastal aquaculture in India. CBS Publishers and Distributors, New Delhi 37. Schreieck M, Wiesche M, Krcmar H (2016) Design and Governance of Platform Ecosystems: Key Concepts and Issues for Future Research. Paper presented at the Twenty-Fourth European Conference on Information Systems (ECIS), İstanbul, Turkey 38. Sidhu SS (1963) Studies on Mangroves. Proc Nat Ar:ad Sd. India 33(B) (part-1):129-136 39. Singh D, Buhmann AK, Flowers TJ, Seal CE, Papenbrock J (2014) Salicornia as a crop plant in temperate regions: selection of genetically characterized ecotypes and optimization of their cultivation conditions. AoB Plants doi:10.1093/aobpla/plu071 40. Smillie C (2015) Salicornia spp. as a biomonitor of Cu and Zn in salt marsh sediments. Ecol Indic 56:70–78 41. Tanaka T (1976) Tanaka’s Cyclopedia of Edible Plants of the World, Keigaku Publishing Co., Tokyo 42. Tang DL, Kawamura H (2001) Long-term series satellite ocean colour products on the Asian waters. In: Proceedings of the 11th PAMS/JECSS workshop. Hanrimwon Publishing (CD-ROM: 0112-PO3), Seoul, pp. 49–52 43. UNEP (1985) Environmental problems of marine and coastal area of India. UNEP Regional seas Reports and Studies No 59 44. Williams D (2002) Management options for the shrimp fry fishery, Regional stakeholder workshop in Khulna, Bangladesh 8 45. Yamamoto K, Oguri S, Chiba S., Momonoki YS (2009) Molecular cloning of acetylcholinesterase gene from Salicornia europaea L. Plant Signal Behav 4:361–366 46. Zaman S, Biswas S, Pal N, Datta U, Biswas P, Mitra A (2016) Ecosystem Service of Heritiera fomes Seedlings in terms of Carbon Storage. Int J Trend Res Dev 3(4):183-185
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ÖNSÖZ ve ÖZET Türkiye Odalar ve Borsalar Birliği (TOBB), İklimlendirme Meclisi (İM) tarafından kurulan İç Hava Kalitesi Komisyonu, Türkiye için geliştirilecek iç hava kalitesi yönetmeliğine öneri geliştirmek üzere bir İHK - Yönetmelik Limit Değerler Çalışma Grubu oluşturmuştur. Çeşitli üniversitelerden akademisyenlerin ve uzmanların oluşturduğu Çalışma Grubu ilk olarak, okullarda/sınıflarda iç hava kirleticilerinin öğrenci sağlığını etkilemeyecek limit değerlerini önermeyi, ilk hedef olarak belirlemiş ve kendi içinde iç hava kirleticileri için iş bölümü yapmıştır. Bu kitap, Çalışma Grubu içinde yer alan Macit Toksoy ve Sait Cemil Sofuoğlu tarafından sınıf - karbon dioksit – öğrenci arakesiti üzerinde, mevcut Literatürün değerlendirilmesi ile yapılan çalışmanın ürünüdür. Çalışma hem sınıflardaki müsaade edilebilir karbon dioksit konsantrasyonları ile ilgili önerileri geliştirmek hem de sınıflarda yapılacak havalandırma sistemları tasarımı kriterleri için bir referans doküman oluşturmak hedefiyle gerçekleştirilmiştir. Giderek yoğunlaşan araştırmalar, tüm dünyadaki okullarda büyük bir çoğunlukla yeterli havalandırmanın yapılmadığını, sınıflardaki iç hava kalitesinin çocukların fiziksel ve zihinsel (bilişsel) sağlığını ve performansını etkiler durumda olduğunu göstermektedir. COVID-19 salgını ile birlikte çocukların maruz kaldıkları gaz ve partikül kirliliklerinin yanında, havada asılı hastalık yapan biyolojik partikülleri (patojenlerin) iç hava kirliliğine, havalandırma tasarımı ve uygulaması perspektifinden yeni bir boyut değil ama bu boyuta ciddi bir derinlik kazandırmıştır. Yapılan araştırmalar, yeni yapılmış veya yeniden düzenlenmiş okullarda bile havalandırma sistemlerinin istenilen iç hava kalitesini sağlamada başarısız kaldıklarını göstermiştir. Bu başarısızlığın sebepleri tasarımda yetersizlik, uygun olmayan işletme, okul ve bina topluluklarında iç hava kalitesi konusunda eğitimsizlik olarak belirtilmiştir. Günümüzde gelinen nokta itibariyle, en başta mühendislik pratiği açısından tasarıma, uygulamaya ve denetime daha geniş bir perspektifte rehberlik edecek şekilde bir havalandırma tanımı yapmayı gerektirmektedir. Bu çalışmada dış ve iç havada (sınıflarda) karbondioksit konsantrasyonları, insan ve öğrenci sağlığı üzerine etkileri incelenmiş, havalandırma tanımı yapılmış ve karbon dioksitin havalandırma tasarımı açısından önemi üzerinde durulmuştur. Nihai olarak da, göz önüne alınan ve değerlendirilen literatürün ışığında sınıflarda, çocukların fizyolojik sağlığı, bilişsel performansı ve akademik başarısı için, antropolojik metrikler göz önünde tutularak, CO2 konsantrasyonunu ortalama 800 ppm’de tutacak havalandırma debisi sağlanması, dış hava CO2 konsantrasyonu göz önüne alınarak ve sınıfta konsantrasyonunun 1000 ppm’in üzerine çıkmaması ölçütleriyle havalandırma sistem tasarımının yapılması önerilmiştir. Bu tasarımın tam olarak yapılabilmesi için de özellikle okulların çevresinde, zamana bağlı CO2 dahil dış hava kirlilik haritalarının çıkarılması çok önemlidir. Önerilen 800 ppm – 1000 ppm değeri mutlak değerlerdir ve havalandırma sistemi tasarımı yapılırken okulun bulunduğu bölgenin CO2 konsantrasyonu değişimleri göz önüne alınmalıdır.
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Relatively high indoor CO2 concentration (>1000 ppm) has a negative impact on human health. In this work, a cost-effective CO2 adsorbent (DKOH-AC) was developed by impregnating KOH on rice husk-based KOH activated carbon (KOH-AC, 1439 m²/g). KOH can be successfully loaded on the surface of KOH-AC and significantly changed its surface properties. DKOH-AC still remained a considerable surface area (206 m²/g) and showed a similar Smicro/SBET ratio. In-situ FTIR analysis confirmed that the major CO2 adsorption mechanism of KOH-AC was based on physisorption while that on DKOH-AC involved both chemisorption and physisorption. DKOH-AC showed a higher heat of adsorption (34 ∼ 41 KJ/mol) and gas selectivity (16.6) than these of KOH-AC. KOH-AC quickly reached an adsorption equilibrium (about 50 min) as compared to that of DKOH-AC. In addition, DKOH-AC exhibited an excellent adsorption performance of 2.1 mmol/g for a low concentration of CO2 (2000 ppm ∼ 500 ppm) under indoor conditions. Both the CO2 adsorption isotherm on KOH-AC and DKOH-AC well followed the Langmuir and Freundlich models. The CO2 adsorption kinetics on KOH-AC followed the pseudo-first order model whereas that on DKOH-AC obeyed the pseudo-second order model. The adsorption process was controlled by the intraparticle diffusion combined with the film diffusion model.
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Protein transcription, translation, and folding occur continuously in every living cell and are essential for physiological functions. About one-third of all proteins of the cellular proteome interacts with the endoplasmic reticulum (ER). The ER is a large, dynamic cellular organelle that orchestrates synthesis, folding, and structural maturation of proteins, regulation of lipid metabolism and additionally functions as a calcium store. Recent evidence suggests that both acute and chronic hypercapnia (elevated levels of CO 2 ) impair ER function by different mechanisms, leading to adaptive and maladaptive regulation of protein folding and maturation. In order to cope with ER stress, cells activate unfolded protein response (UPR) pathways. Initially, during the adaptive phase of ER stress, the UPR mainly functions to restore ER protein-folding homeostasis by decreasing protein synthesis and translation and by activation of ER-associated degradation (ERAD) and autophagy. However, if the initial UPR attempts for alleviating ER stress fail, a maladaptive response is triggered. In this review, we discuss the distinct mechanisms by which elevated CO 2 levels affect these molecular pathways in the setting of acute and chronic pulmonary diseases associated with hypercapnia.
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The Neurovascular Unit (NVU) is an important multicellular structure of the central nervous system (CNS), which participates in the regulation of cerebral blood flow (CBF), delivery of oxygen and nutrients, immunological surveillance, clearance, barrier functions, and CNS homeostasis. Stroke and Alzheimer Disease (AD) are two pathologies with extensive NVU dysfunction. The cell types of the NVU change in both structure and function following an ischemic insult and during the development of AD pathology. Stroke and AD share common risk factors such as cardiovascular disease, and also share similarities at a molecular level. In both diseases, disruption of metabolic support, mitochondrial dysfunction, increase in oxidative stress, release of inflammatory signaling molecules, and blood brain barrier disruption result in NVU dysfunction, leading to cell death and neurodegeneration. Improved therapeutic strategies for both AD and stroke are needed. Carbonic anhydrases (CAs) are well-known targets for other diseases and are being recently investigated for their function in the development of cerebrovascular pathology. CAs catalyze the hydration of CO2 to produce bicarbonate and a proton. This reaction is important for pH homeostasis, overturn of cerebrospinal fluid, regulation of CBF, and other physiological functions. Humans express 15 CA isoforms with different distribution patterns. Recent studies provide evidence that CA inhibition is protective to NVU cells in vitro and in vivo, in models of stroke and AD pathology. CA inhibitors are FDA-approved for treatment of glaucoma, high-altitude sickness, and other indications. Most FDA-approved CA inhibitors are pan-CA inhibitors; however, specific CA isoforms are likely to modulate the NVU function. This review will summarize the literature regarding the use of pan-CA and specific CA inhibitors along with genetic manipulation of specific CA isoforms in stroke and AD models, to bring light into the functions of CAs in the NVU. Although pan-CA inhibitors are protective and safe, we hypothesize that targeting specific CA isoforms will increase the efficacy of CA inhibition and reduce side effects. More studies to further determine specific CA isoforms functions and changes in disease states are essential to the development of novel therapies for cerebrovascular pathology, occurring in both stroke and AD.
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Carbonic anhydrases (CAs) catalyze the synthesis of HCO3⁻ from H2O and CO2. The dysfunction of CAs leads to aqueous humor secretion and high intraocular pressure to cause glaucoma pathogenesis. Methazolamide (MTZ), a CA inhibitor, can effectively treat glaucoma by reducing aqueous humor secretion. We previously reported that carbonic anhydrase I (CA1), a CA family member, was highly expressed in atherosclerotic tissues of the aorta and stimulated atherosclerosis (AS) by promoting calcification. MTZ showed therapeutic and preventive effects on AS in a mouse model. The above findings suggest a relationship between AS and glaucoma. This study explored the possible association between AS prevalence and glaucoma prevalence and the therapeutic effect of MTZ on AS by analyzing medical records. Among 10,751 patients with a primary diagnosis of glaucoma, 699 (6.5%) were also diagnosed with AS. However, the incidences of AS in patients with keratitis and scleritis, which are also ophthalmic diseases, were 2.5% (206/8383 patients) and 3.5% (46/1308 patients), respectively. In the population without ophthalmic records, the AS prevalence was only 1.9% (99,416/5,168,481 patients) (all p values between each group were below 0.001). Among 152,425 patients with a primary diagnosis of AS, 1245 (0.82%) were also diagnosed with glaucoma. Among 199,782 patients with a primary diagnosis of hypertension (excluding AS), 1149 (0.57%) were diagnosed with glaucoma, and among 5,313,433 patients without AS or hypertension, 9513 (0.18%) were diagnosed with glaucoma (all p values between each group were below 0.001). Additionally, among 14 patients who suffered from both AS and glaucoma and were treated with MTZ to cure their glaucoma, 9 of them showed reduced low-density lipoprotein (LDL) levels, the main index of AS, within 3 months after medication use (2.81 ± 0.61 mmol/L vs. 2.38 ± 0.58 mmol/L, p = 0.039). The above findings demonstrated a strong relation between AS and glaucoma and suggested that AS patients with glaucoma were more likely to suffer from angle-closure glaucoma.
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Key points: Long-term exposure to elevated levels of atmospheric CO2 is an uncontrolled experiment already underway. This is the first known study to assess non-respiratory physiological impacts of long-term (conception to young adulthood) exposure of mice to CO2 at levels that may arise in the atmosphere due to global emissions. Exposure to elevated CO2 , in comparison to control mice, altered growth patterns in early life and resulted in hyperactive behaviours in young adulthood. Renal and bone parameters, which are important to balance acid-base levels to compensate for increased CO2 exposure, remained relatively unaffected. This work adds to the body of evidence regarding the effects of carbon emissions on mammalian health and highlights a potential future burden of disease. Abstract: Atmospheric carbon dioxide (CO2 ) levels are currently at 418 parts per million (ppm), and by 2100 may exceed 900 ppm. The biological effects of lifetime exposure to CO2 at these levels is unknown. Previously we have shown that mouse lung function is altered by long-term exposure to 890 ppm CO2 . Here, we assess the broader systemic physiological responses to this exposure. Mice were exposed to either 460 ppm or 890 ppm from preconception to 3 months of age, and assessed for effects on developmental, renal, and osteological parameters. Locomotor, memory, learning, and anxiety-like behaviours of the mice were also assessed. Exposure to 890 ppm CO2 increased birthweight, decreased female body weight after weaning, and, as young adults, resulted in reduced engagement in memory/learning tasks, and hyperactivity in both sexes in comparison to controls. There were no clear anxiety, learning, or memory changes. Renal and osteological parameters were minimally affected. Overall, this study shows that exposure of mice to 890 ppm CO2 from preconception to young adulthood alters growth and some behaviours, with limited evidence of compensatory changes in acid-base balance. These findings highlight the potential for a direct effect of increased atmospheric CO2 on mammalian health outcomes. Abstract figure. The aim of this study is to investigate how rising atmospheric carbon dioxide (CO2 ) levels affect mouse physiology. To achieve this, mice were exposed to either 460 ppm (standard housing conditions) or 890 ppm (may eventuate by 2100) from preconception to 3 months of age. Mice were assessed for effects on developmental, renal, osteological, and behavioural parameters. Exposure to 890 ppm CO2 increased birthweight, decreased female body weight after weaning, and, as young adults, resulted in reduced engagement in memory/learning tasks, and hyperactivity in both sexes in comparison to controls. There were no clear anxiety, learning, or memory changes. Renal and osteological parameters were minimally affected. Overall, this study shows that exposure of mice to 890 ppm CO2 from preconception to young adulthood alters growth and some behaviours, with limited evidence of compensatory changes in acid-base balance. While more work needs to be done, these findings highlight the potential for a direct effect of increased atmospheric CO2 on mammalian health outcomes. This article is protected by copyright. All rights reserved.
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This volume assembles and integrates the wealth of diverse information that is now accumulating in this burgeoning field. The existing and potential therapeutic applications of targeting CA cover a remarkably wide-range of diseases and disorders and have generated increasing and extensive interest in recent years. Its inter-disciplinary approach embraces both the most up-to-date therapeutic application of CA-targeting and the latest research data that will provide a platform for the development of novel applications. The interested audience comprises scientists and clinicians from many relevant disciplines within science and medicine.
Chapter
Carbonic anhydrases (CAs) are widely expressed in the nervous system where they play important physiological roles. In the brain and other parts of the system, different isozymes show unique distribution patterns, some of them being present in neurons (CA II, V, VII, XIV), capillary endothelium (CA IV), microglia (CA III), choroid plexus (CA II, III, XII, XIV), astrocytes (CA II and V), oligodendrocytes (CA II and XIII), and myelin sheath (CA II). Nervous tissues also express three carbonic anhydrase-related proteins (CARP VIII, X, XI), which may be involved in the brain development processes. Future research is needed to define the exact roles of these highly conserved CA isoforms and to design novel treatment strategies for the diseases caused by defects or abnormal regulation of CARPs. Enzymatically active CA isozymes are known drug targets to treat various neurological disorders including epilepsy, acute mountain sickness, pseudotumor cerebri, and brain edema. In this review article, we describe how the clinically approved CA inhibitors are used for the treatment of these diseases.
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Carbon dioxide (CO 2 ) is a fundamental physiological gas known to profoundly influence the behaviour and health of millions of species within the plant and animal kingdoms in particular. A recent Royal Society meeting on the topic of ‘Carbon dioxide detection in biological systems' was extremely revealing in terms of the multitude of roles that different levels of CO 2 play in influencing plants and animals alike. While outstanding research has been performed by leading researchers in the area of plant biology, neuronal sensing, cell signalling, gas transport, inflammation, lung function and clinical medicine, there is still much to be learned about CO 2 -dependent sensing and signalling. Notably, while several key signal transduction pathways and nodes of activity have been identified in plants and animals respectively, the precise wiring and sensitivity of these pathways to CO 2 remains to be fully elucidated. In this article, we will give an overview of the literature relating to CO 2 -dependent signal transduction in mammalian systems. We will highlight the main signal transduction hubs through which CO 2 -dependent signalling is elicited with a view to better understanding the complex physiological response to CO 2 in mammalian systems. The main topics of discussion in this article relate to how changes in CO 2 influence cellular function through modulation of signal transduction networks influenced by pH, mitochondrial function, adenylate cyclase, calcium, transcriptional regulators, the adenosine monophosphate-activated protein kinase pathway and direct CO 2 -dependent protein modifications. While each of these topics will be discussed independently, there is evidence of significant cross-talk between these signal transduction pathways as they respond to changes in CO 2 . In considering these core hubs of CO 2 -dependent signal transduction, we hope to delineate common elements and identify areas in which future research could be best directed.
Article
Background: Climate change models predict that atmospheric carbon dioxide [CO2] levels will be between 700 and 900 ppm within the next 80 y. Despite this, the direct physiological effects of exposure to slightly elevated atmospheric CO2 (as compared with ∼410 ppm experienced today), especially when exposures extend from preconception to adulthood, have not been thoroughly studied. Objectives: In this study we aimed to assess the respiratory structure and function effects of long-term exposure to 890 ppm CO2 from preconception to adulthood using a mouse model. Methods: We exposed mice to CO2 (∼890 ppm) from prepregnancy, through the in utero and early life periods, until 3 months of age, at which point we assessed respiratory function using the forced oscillation technique, and lung structure. Results: CO2 exposure resulted in a range of respiratory impairments, particularly in female mice, including higher tissue elastance, longer chord length, and lower lung compliance. Importantly, we also assessed the lung function of the dams that gave birth to our experimental subjects. Even though these mice had been exposed to the same level of increased CO2 for a similar amount of time (∼8wk), we measured no impairments in lung function. This suggests that the early life period, when lungs are undergoing rapid growth and development, is particularly sensitive to CO2. Discussion: To the best of our knowledge, this study, for the first time, shows that long-term exposure to environmentally relevant levels of CO2 can impact respiratory function in the mouse. https://doi.org/10.1289/EHP7305.
Article
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