David Kattari’s scientific contributions

Objective The purpose of this study was to determine if the COVID-19 pandemic had differential effects on individuals with chemical intolerances (CI). CI is characterised by multisystem symptoms initiated by a one-time high dose or persistent low-dose exposure to environmental toxins including chemicals, foods and drugs. With an estimated 20% US prevalence, symptoms include fatigue, headache, weakness, rash, mood changes, musculoskeletal pain, gastrointestinal issues, difficulties with memory, concentration and respiratory problems, which are similar to COVID-19 and its sequelae. Design A US population-based survey involving 7500 respondents was asked if they ever had COVID-19, what the severity was, and if they had long COVID-19. CI was assessed using the Quick Environmental Exposure and Sensitivity Inventory. Setting The Center for Disease Control estimates that over 24 million have been infected with COVID-19 in the USA with over 6 700 000 being hospitalised and over 1 174 000 deaths. Other industrialised countries show similar numbers. Results Those in the High CI class reported a greater COVID-19 prevalence, symptom severity and long COVID-19 than in the medium and low CI groups (p<0.0001). These associations were independent of race, ethnicity, income, age and sex. However, there were significantly increased odds of COVID-19 severity among women and those over 45 years old. Asian individuals were least likely to have severe symptoms compared with white individuals (OR=0.53; 95% CI 0.35 to 0.79). Black/African American individuals reported a lower prevalence of COVID-19 than non-Hispanic whites. However, one interaction between CI and race was significant, African Americans with high CI reported greater odds (OR=2.2; 95% CI 1.15 to 3.16) of reporting COVID-19 prevalence. Furthermore, African American individuals had significantly greater odds of increased symptom severity. Conclusion Prior studies show higher risk for COVID-19 among older age groups, male sex, those with pre-existing comorbidities (eg, challenged immunities) and those from minoritised racial/ethnic groups. The results of this study suggest that those with CI be included in a high-risk group. Various risk subsets may exist and future investigations could identify different risk subsets. Understanding these subgroups would be helpful in mounting targeted prevention efforts.

Background The Center for Disease Control has estimated that over 24 million have been infected with COVID-19 in the US with over 6,700,000 being hospitalized, and over 1,174,000 deaths. Several other industrialized countries show similar numbers (CSSE, 2021). Chemical Intolerance (CI) is characterized by multi-system symptoms initiated by a one-time high dose or persistent low-dose exposure to environmental toxins including chemicals, foods and drugs. With an estimated 20% prevalence in the US, the symptoms of CI include fatigue, headache, weakness, rash, mood changes, musculoskeletal pain, gastrointestinal issues, difficulties with memory, concentration, and respiratory problems which are similar to COVID-19 and its sequelae. The purpose of this study was to determine if the pandemic had differential effects on those individuals with CI. Methods A large U.S. population-based survey was launched involving 7,500 respondents asking if they ever had COVID-19, what the severity of it was, and if they have long COVID-19. Respondents were also assessed for CI using the Quick Environmental Exposure and Sensitivity Inventory (QEESI), a 50-item validated questionnaire designed to assess intolerances to inhaled chemicals, foods, and/or drugs. Respondents were classified as Low, Medium, or High CI. Results Those in the High Chemical Intolerance class reported a greater COVID-19 prevalence, symptom severity, and long COVID-19 then in the Medium and Low CI classes (P<.0001). These associations were independent of race, ethnicity, income, age, and gender. However, there was significantly increased odds of COVID-19 severity among females and those over 45 years old. Asian individuals were least likely to have severe symptoms compared to White individuals (OR = 0.60). Black/African American individuals reported a lower prevalence of COVID-19 than Non-Hispanic Whites (NHW), but African American individuals with high CI reported 2.2 greater odds of reporting COVID-19 prevalence. Further, African American individuals had significantly greater odds of increased symptom severity. Discussion Prior studies showed that higher risk for COVID-19-19 infection include the elderly, male sex, those with pre-existing comorbidities (e.g., challenged immunities) and those from minoritized racial/ethnic groups. The results of this study suggest that those with CI be included in a high risk group. Various risk subsets may exisit and future investigations could identify different risk subsets. Understanding these subgroups would be helpful in mounting targeted prevention efforts.

Background: We sought to replicate our 2015 findings linking chemical intolerance in parents with the risk of their children developing autism and/or ADHD. Drawing upon our 2021 discovery of a strong association between chemical intolerance and mast cells, we propose an explanation for this link. Methods: In a population-based survey of U.S. adults, we used the internationally validated Quick Environmental Exposure and Sensitivity Inventory (QEESI) to assess symptom severity and chemical intolerance. Parents were asked how many of their biological children had been diagnosed with autism and/or ADHD. Results: Parents with chemical intolerance scores in the top versus bottom tenth percentile had 5.7 times the risk of reporting a child with autism and 2.1 times for ADHD. Conclusions: High chemical intolerance scores among parents of children with autism, coupled with our 2021 discovery of mast cell activation as a plausible biomechanism for chemical intolerance, suggest that (1) the QEESI can identify individuals at increased risk, (2) environmental counseling may reduce personal exposures and risk, and (3) the global rise in autism and ADHD may be due to fossil-fuel-derived and biogenic toxicants epigenetically “turning on” or “turning off” critical mast cell genes that can be transmitted transgenerationally. It is important to note that this study was observational in nature; as such, further research is needed using controlled trials to confirm causality and explore the proposed mechanism.

Background Worldwide observations point to a two-stage theory of disease called Toxicant-Induced Loss of Tolerance (TILT): Stage I, Initiation by an acute high-level or repeated lower-level chemical exposures, followed by Stage II, Triggering of multisystem symptoms by previously tolerated, structurally diverse chemical inhalants, foods/food additives and drugs. Until recently, there was no known biological mechanism that could explain these observations. In 2021, we published a plausible and researchable two-stage biomechanism for TILT involving mast cells: Stage I, Initiation via mast cell sensitization; Stage II, Triggering of mast cell degranulation by previously tolerated exposures, resulting in the release of thousands of mediators, including histamine and a host of inflammatory molecules. The objective of this study was to identify common TILT initiators. Methods A randomized, population-based sample of 10,981 U.S. adults responded to a survey which included items concerning medical diagnoses, personal exposures, antibiotic use, and several possible initiators of Chemical Intolerance (CI). CI was assessed using the internationally validated Quick Environmental Exposure and Sensitivity Inventory (QEESI). Participants identified as chemically intolerant were asked to recall when their intolerances began and what they felt had initiated their condition. Results Twenty percent met QEESI criteria for TILT, approximately half of whom identified one or more initiating exposures. Initiators in order of frequency were mold (15.6%), pesticides (11.5%), remodeling/new construction (10.7%), medical/surgical procedures (11.3%), fires/combustion products (6.4%), and implants (1.6%). Protracted antibiotic use for infections involving the prostate, skin, tonsils, gastrointestinal tract, and sinuses were strongly associated with TILT/CI (OR > 2). Discussion Participants identified two broad classes of TILT initiators: 1) fossil fuel-derived toxicants (i.e., from coal, oil, natural gas), their combustion products, and/or synthetic organic chemical derivatives, e.g., pesticides, implants, drugs/antibiotics, volatile organic compounds (VOCs); and 2) biogenic toxicants, e.g., particles and VOCs from mold or algal blooms. One in four primary care patients suffers from Medically Unexplained Symptoms (MUS). Doctors in primary care, neurology, psychiatry, psychology, occupational medicine, and allergy/immunology would be well-advised to include TILT in their differential diagnosis of patients with so-called MUS. Because 20% of U.S. adults meet QEESI criteria for CI, the role of contemporary exposures in initiating and exacerbating these conditions via mast cells needs our immediate attention. There is a concomitant need for policies and practices that reduce initiating exposures as well as ubiquitous and often unavoidable triggers such as fragranced personal care, cleaning, and laundry products in multi-occupant housing, workplaces, medical settings, schools, places of worship, and all public buildings—literally anywhere air is shared. Fossil fuels are assaulting humans and other animal species both from within via mast cell sensitization, and from without via climate change.

Background Worldwide observations point to a two-stage theory of disease called Toxicant-Induced Loss of Tolerance (TILT): Stage I, Initiation by an acute high-level or repeated lower-level chemical exposures, followed by Stage II, Triggering of multisystem symptoms by previously tolerated, structurally diverse chemical inhalants, foods/food additives and drugs. Until recently, there was no known biological mechanism that could explain these observations. In 2021 we published a plausible and researchable two-stage biomechanism for TILT involving mast cells: Stage I, Initiation via mast cell sensitization; Stage II, Triggering of mast cell degranulation by previously tolerated exposures, resulting in the release of thousands of mediators, including histamine and a host of inflammatory molecules. The objective of this study was to identify common TILT initiators. Methods A randomized, population-based sample of 10,981 U.S. adults responded to a survey which included items concerning medical diagnoses, personal exposures, antibiotic use, and several possible initiators of Chemical Intolerance (CI). CI was assessed using the internationally validated Quick Environmental Exposure and Sensitivity Inventory (QEESI). Participants identified as chemically intolerant were asked to recall when their intolerances began and what they felt had initiated their condition. Results Twenty percent met QEESI criteria for TILT, approximately half of whom identified one or more initiating exposures. Initiators in order of frequency were mold (15.6%), pesticides (11.5%), remodeling/new construction (10.7%), medical/surgical procedures (11.3%), fires/combustion products (6.4%), and implants (1.6%). Protracted antibiotic use for infections involving the prostate, skin, tonsils, gastrointestinal tract, and sinuses were strongly associated with TILT/CI (OR > 2). Discussion Participants identified two broad classes of TILT initiators: 1) fossil fuel-derived toxicants (i.e., from coal, oil, natural gas), their combustion products, and/or synthetic organic chemical derivatives, e.g., pesticides, implants, drugs/antibiotics, volatile organic compounds (VOCs), and 2) biogenic toxicants, e.g., particles and VOCs from mold or algal blooms. One in four primary care patients suffers from Medically Unexplained Symptoms (MUS). Doctors in primary care, neurology, psychiatry, psychology, occupational medicine, and allergy/immunology would be well-advised to include TILT in their differential diagnosis of patients with so-called MUS. Because 20% of U.S. adults meet QEESI criteria for CI, the role of contemporary exposures in initiating and exacerbating these conditions via mast cells needs our immediate attention. There is a concomitant need for policies and practices that reduce initiating exposures as well as ubiquitous and often unavoidable triggers such as fragranced personal care, cleaning, and laundry products in multi-occupant housing, workplaces, medical settings, schools, places of worship, and all public buildings—literally anywhere air is shared. Fossil fuels are assaulting humans and other animal species both from withinvia mast cell sensitization, and from without via climate change.

Background: Chemical intolerance (CI) is characterized by multisystem symptoms triggered by low levels of exposure to xenobiotics including chemicals, foods/food additives, and drugs/medications. Prior prevalence estimates vary from 8-33% worldwide. Clinicians and researchers need a brief, practical screening tool for identifying possible chemical intolerance. This large, population-based study describes the validation of a three-item screening questionnaire, the Brief Environmental Exposure and Sensitivity Inventory (BREESI), against the international reference standard used for assessing chemical intolerance, the Quick Environmental Exposure and Sensitivity Inventory (QEESI). Methods: More than 10,000 people in the U.S. responded to the BREESI and the QEESI in a population-based survey. We calculated the overall prevalence of CI in this sample, as well as by gender, age, and income. Common statistical metrics were used to evaluate the BREESI as a screener for CI against the QEESI. Results: The prevalence estimate for QEESI-defined chemical intolerance in the U.S. was 20.39% (95% CI 19.63-21.15%). The BREESI had 91.26% sensitivity (95% CI: 89.20-93.04%) and 92.89% specificity (95% CI: 91.77-93.90%). The positive likelihood ratio was 12.83 (95% CI: 11.07-14.88), and the negative likelihood ratio was 0.09 (95% CI: 0.08-0.12). Logistic regression demonstrates that the predicted probability of CI increased sharply with each increase in the number of BREESI items endorsed (Odds Ratio: 5.3, 95% CI: 4.90-5.75). Conclusions: Chemical intolerance may affect one in five people in the U.S. The BREESI is a new, practical instrument for researchers, clinicians, and epidemiologists. As a screening tool, the BREESI offers a high degree of confidence in case ascertainment. We recommend: screen with the BREESI, confirm with the QEESI.

Keywords: Chemical Intolerance, Drug Intolerance, Food Intolerance, QEESI, BREESI, Multiple Chemical Sensitivity, Toxicant-induced Loss of Tolerance, Prevalence