Lung cancer risk among female textile workers exposed to endotoxin.
ABSTRACT Reduced risk of lung cancer among workers in the cotton textile industry has been observed since the 1970s. Bacterial endotoxin, a contaminant of raw cotton fiber and cotton dust, has been proposed as a protective agent that may act through the innate and acquired immune systems. We examine the association between endotoxin exposure and lung cancer risk in a cohort of female textile workers.
We conducted a case-cohort study nested within a cohort of 267,400 female textile workers in Shanghai, China. We compared the cumulative exposure histories of 628 case patients diagnosed with incident lung cancer from January 1, 1989, through December 31, 1998, with those of a lung cancer-free reference subcohort of 3184 workers who were frequency matched by 5-year age-groups to all cancer patients in the cohort. Cumulative endotoxin exposure for all participants was based on historic measurements and on additional measurements for this study. Relative risks and 95% confidence intervals (CIs) were estimated by hazard ratios (HRs) from Cox proportional hazards models. We conducted exposure-response trend analyses by use of cumulative exposures with lag times of 0, 5, 10, 15, or 20 years to account for disease latency. All analyses controlled for age and smoking status. All statistical tests were two-sided.
Cumulative exposure to endotoxin was strongly, statistically significantly, and inversely associated with lung cancer risk. The inverse trend was greatest with a 20-year lag time, for which highest endotoxin exposure was associated with a statistically significantly 40% less risk of lung cancer (HR = 0.60, 95% CI = 0.43 to 0.83; P(trend) across quintiles = .002) than non-exposure. From a reported population rate of lung cancer among women in Shanghai of 19.1 per 100,000 for the year 2000 and the estimated reduction in risk of lung cancer observed for 20 years of endotoxin exposure in this population of workers, the incidence of lung cancer in this cohort was reduced by approximately 7.6 per 100,000 (range = 3.2-10.9 per 100,000).
Long-term and high-level exposure to endotoxin, compared with no exposure, appears to be associated with a reduced risk of lung cancer in this cohort.
Article: Human Lung Cancer Risks from Radon - Part III - Evidence of Influence of Combined Bystander and Adaptive Response Effects on Radon Case-Control Studies - A Microdose Analysis.[show abstract] [hide abstract]
ABSTRACT: Since the publication of the BEIR VI (1999) report on health risks from radon, a significant amount of new data has been published showing various mechanisms that may affect the ultimate assessment of radon as a carcinogen, in particular the potentially deleterious Bystander Effect (BE) and the potentially beneficial Adaptive Response radio-protection (AR). The case-control radon lung cancer risk data of the pooled 13 European countries radon study (Darby et al 2005, 2006) and the 8 North American pooled study (Krewski et al 2005, 2006) have been evaluated. The large variation in the odds ratios of lung cancer from radon risk is reconciled, based on the large variation in geological and ecological conditions and variation in the degree of adaptive response radio-protection against the bystander effect induced lung damage. The analysis clearly shows Bystander Effect radon lung cancer induction and Adaptive Response reduction in lung cancer in some geographical regions. It is estimated that for radon levels up to about 400 Bq m(-3) there is about a 30% probability that no human lung cancer risk from radon will be experienced and a 20% probability that the risk is below the zero-radon, endogenic spontaneous or perhaps even genetically inheritable lung cancer risk rate. The BEIR VI (1999) and EPA (2003) estimates of human lung cancer deaths from radon are most likely significantly excessive. The assumption of linearity of risk, by the Linear No-Threshold Model, with increasing radon exposure is invalid.Dose-Response 01/2012; 10(3):415-61. · 1.91 Impact Factor
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ABSTRACT: A recent systematic review and meta-analysis suggested that occupational exposure to endotoxins protects against lung cancer. To explore this hypothesis further, the follow-up of mortality of a cohort of 3551 workers, who were employed in the British cotton industry during 1966-1971, was extended by 23 years. Subjects had originally been recruited to a survey of respiratory disease, which collected information about occupation and smoking habits. Cumulative exposures to endotoxins were estimated from data on endotoxin levels by work areas in cotton mills. Risks of lung cancer were estimated using survival modelling. During follow-up, 2018 deaths were recorded before the age of 90 years, including 128 deaths from lung cancer. After adjustment for smoking, hazard ratios (95% confidence intervals) for cumulative endotoxin exposures of ≤30,000, >30,000 and ≤200,000, >200,000 and ≤400,000, >400,000 and ≤600,000 and >600,000 endotoxin units (EU) m(-3) years were 1, 0.8 (0.5-1.6), 0.7 (0.4-1.3), 0.6 (0.3-1.0) and 0.5 (0.3-0.9), respectively (P for trend=0.005). Our findings strengthen the evidence that occupational exposure to endotoxins protects against lung cancer, and suggest that the effect depends on cumulative dose and persists after exposure ceases.British Journal of Cancer 08/2011; 105(7):1054-60. · 5.04 Impact Factor
Article: Reproductive history and mortality from cardiovascular disease among women textile workers in Shanghai, China.[show abstract] [hide abstract]
ABSTRACT: Few studies have examined the possible effects of reproductive factors on cardiovascular disease (CVD) risks in Asian women. A cohort of 267,400 female textile workers in Shanghai, China, was administered a questionnaire at enrolment (1989-91) and followed for mortality through 2000. Relative risks (hazard ratios) for ischaemic heart disease (IHD), ischaemic stroke and haemorrhagic stroke were calculated using Cox proportional hazards modelling, adjusting for relevant co-variates. Risks were not consistently associated with age at menopause, parity, stillbirths, miscarriages or duration of lactation. An increasing trend in IHD mortality risk, but not stroke, was observed with decreasing age at menarche. There was no evidence of increased CVD mortality risk by oral or injectable contraceptive use or induced abortions. As expected, greater mortality rates from CVD and increased CVD risks were also observed with smoking. Use of steroid contraceptives, induced abortions and reduced parity from China's one-child-per-family policy has not had an adverse effect on risk of CVD mortality in this cohort.International Journal of Epidemiology 12/2011; 40(6):1510-8. · 6.41 Impact Factor