Lack of a protective effect of cotton dust on risk of lung cancer: evidence from two population-based case-control studies.

BACKGROUND: Lung cancer is the leading cause of cancer death in North America. Exposure to cotton dust has previously been reported to decrease the risk of lung cancer. METHODS: We used data from two large case-control studies conducted in Montreal from 1979-1986 (Study 1) and 1996-2002 (Study 2) respectively, to examine the association between occupational exposure to cotton dust and risk of lung cancer. Cases were diagnosed with incident histologically-confirmed lung cancer (857 in Study 1, 1203 in Study 2). Population controls were randomly selected from electoral lists and frequency-matched to cases by age and sex (533 in Study 1, 1513 in Study 2). Interviews for the two studies used a virtually identical questionnaire to obtain lifetime occupational and smoking history, and several lifestyle covariates. Each participant's lifetime occupational history was reviewed by experts to assess exposure to a number of occupational agents, including cotton dust. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by unconditional logistic regression, adjusting for potential confounders. RESULTS: The lifetime prevalence of exposure to cotton dust was approximately 10%-15% in both studies combined, with some variation by study and by sex. Overall there was no decreased risk of lung cancer among subjects exposed to cotton dust. Rather, among all subjects there was a suggestion of slightly increased risk associated with any lifetime exposure to cotton dust (OR = 1.2, 95% CI: 1.0-1.5). This risk appeared to be concentrated among cases of adenocarcinoma (OR = 1.6, 95% CI: 1.2-2.2), and among moderate and heavy smokers (OR = 1.3, 95% CI: 1.0-1.7). There was no association when restricting to cases of either squamous cell or small cell cancer, or among never smokers and light smokers. An analogous examination of subjects exposed to wool dust revealed neither increased nor decreased risks of lung cancer. CONCLUSIONS: There was no evidence that cotton dust exposure decreased risks of lung cancer.

A systematic review of the association between pleural plaques and changes in lung function.

OBJECTIVES: To conduct a systematic review of changes in lung function in relation to presence of pleural plaques in asbestos-exposed populations. METHODS: Database searches of PubMed and Web of Science were supplemented by review of papers' reference lists and journals' tables of contents. Methodological features (eg, consideration of potential confounding by smoking) of identified articles were reviewed by ≥ two reviewers. Meta-analyses of 20 studies estimated a summary effect of the decrements in per cent predicted (%pred) forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) associated with presence of pleural plaques. RESULTS: Among asbestos-exposed workers, the presence of pleural plaques was associated with statistically significant decrements in FVC (4.09%pred, 95% CI 2.31 to 5.86) and FEV1 (1.99%pred, 95% CI 0.22 to 3.77). Effects of similar magnitude were seen when stratifying by imaging type (X-ray or high-resolution CT) and when excluding studies with potential methodological limitations. Undetected asbestosis was considered as an unlikely explanation of the observed decrements. Several studies provided evidence of an association between size of pleural plaques and degree of pulmonary decrease, and presence of pleural plaques and increased rate or degree of pulmonary impairment. CONCLUSIONS: The presence of pleural plaques is associated with a small, but statistically significant mean difference in FVC and FEV1 in comparison to asbestos-exposed individuals without plaques or other abnormalities. From a public health perspective, small group mean decrements in lung function coupled with an increased rate of decline in lung function of the exposed population may be consequential.

Low levels of exposure to libby amphibole asbestos and localized pleural thickening.

OBJECTIVE: To explore the relationship between low levels of exposure to Libby amphibole asbestos (LAA) and pleural abnormalities, specifically localized pleural thickening (LPT). METHODS: Three studies presenting the risks associated with quantitative LAA exposure estimates were reviewed, paying particular attention to lower exposure ranges. RESULTS: Studies reviewed were conducted among workers exposed to LAA at mining and milling operations in Libby, Montana, at a vermiculite processing facility in Marysville, Ohio, and community residents exposed to LAA from a vermiculite processing facility in Minneapolis, Minnesota. Pleural abnormalities were evaluated using radiographs. Despite differences in study populations and design, each study found that cumulative inhalation LAA exposure was associated with increased risk of LPT even at low levels of exposure. CONCLUSIONS: Inhalation exposure to LAA is associated with increased risk of LPT even at the lowest levels of exposure in each study.

Risk of lung cancer associated with six types of chlorinated solvents: results from two case-control studies in Montreal, Canada.

OBJECTIVES: To determine whether exposure to various chlorinated solvents is associated with lung cancer. METHODS: Two case-control studies of occupation and lung cancer were conducted in Montreal, and included 2016 cases and 2001 population controls. Occupational exposure to a large number of agents was evaluated using a combination of subject-reported job history and expert assessment. We examined associations between lung cancer among men and six specific chlorinated solvents and two chemical families (chlorinated alkanes and alkenes). ORs were calculated using unconditional multivariate logistic regression. RESULTS: When the two studies were pooled, there were indications of an increased risk of lung cancer associated with occupational exposure to perchloroethylene (OR(any exposure) 2.5, 95% CI 1.2 to 5.6; OR(substantial exposure) 2.4, 95% CI 0.8 to 7.7) and to carbon tetrachloride (OR(any exposure) 1.2, 95% CI 0.8 to 2.1; OR(substantial exposure) 2.5, 95% CI 1.1 to 5.7). No other chlorinated solvents showed both statistically significant associations and dose-response relationships. ORs appeared to be higher among non-smokers. When the lung cancer cases were separated by histological type, there was a suggestion of differential effects by tumour type, but statistical imprecision and multiple testing preclude strong inferences in this regard. CONCLUSIONS: There were suggestive, albeit inconsistent, indications that exposure to perchloroethylene and carbon tetrachloride may increase the risk of lung cancer. Results for other solvents were compatible with absence of risk.

Risk of selected cancers due to occupational exposure to chlorinated solvents in a case-control study in Montreal.

OBJECTIVE: To evaluate the association between exposure to chlorinated solvents and cancer. METHODS: We conducted a case-control study of occupational exposures and cancer in Montreal, Quebec, Canada, including 3730 cancer cases and 533 population controls. Occupational exposures were derived using a combination of subject-reported job history and expert assessment. We examined the associations between two chemical families and six chlorinated solvents with 11 sites of cancer. RESULTS: The majority of the associations examined were null, although many were based on small numbers. We found two significantly elevated odds ratios (ORs), one between perchloroethylene and prostate cancer (OR = 4.3; 95% CI: 1.4 to 13) and another between trichloroethylene and melanoma (OR = 3.2; 95% CI: 1.0 to 9.9). CONCLUSIONS: There was little evidence of associations between chlorinated solvents and cancer. Limited power precludes strong inferences about absence of risk. We raise hypotheses about two possible associations: perchloroethylene with prostate cancer and trichloroethylene with melanoma.

The risk of lung cancer related to dietary intake of flavonoids.

It has been hypothesized that flavonoids in foods and beverages may reduce cancer risk through antioxidation, inhibition of inflammation, and other antimutagenic and antiproliferative properties. We examined associations between intake of 5 flavonoid subclasses (anthocyanidins, flavan-3-ols, flavones, flavonols, and flavanones) and lung cancer risk in a population-based case-control study in Montreal, Canada (1061 cases and 1425 controls). Flavonoid intake was estimated from a food frequency questionnaire that assessed diet 2 yr prior to diagnosis (cases) or interview (controls). Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression. Overall, total flavonoid intake was not associated with lung cancer risk, the effect being similar regardless of sex and smoking level. However, low flavonoid intake from food, but not from beverages, was associated with an increased risk. The adjusted ORs (95% CIs) comparing the highest vs. the lowest quartiles of intake were 0.63 (0.47-0.85) for total flavonoids, 0.82 (0.61-1.11) for anthocyanidins, 0.67 (0.50-0.90) for flavan-3-ols, 0.68 (0.50-0.93) for flavones, 0.62 (0.45-0.84) for flavonols, and 0.70 (0.53-0.94) for flavanones. An inverse association with total flavone and flavanone intake was observed for squamous cell carcinoma but not adenocarcinoma. In conclusion, low flavonoid intake from food may increase lung cancer risk.

Maternal concentrations of polyfluoroalkyl compounds during pregnancy and fetal and postnatal growth in British girls.

BACKGROUND: Prenatal exposures to polyfluoroalkyl compounds (PFCs) may be associated with adverse changes in fetal and postnatal growth. OBJECTIVE: We explored associations of prenatal serum concentrations of perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), and perfluorohexane sulfonate (PFHxS) with fetal and postnatal growth in girls. METHODS: We studied a sample of 447 singleton girls and their mothers participating in the Avon Longitudinal Study of Parents and Children (ALSPAC). Data on weight and length were obtained at birth and at 2, 9, and 20 months. Serum samples were obtained in 1991-1992, from mothers during pregnancy. We explored associations between prenatal PFC concentrations and weight at birth as well as longitudinal changes in weight-for-age SD scores between birth and 20 months. RESULTS: PFOS (median, 19.6 ng/mL), PFOA (median, 3.7 ng/mL), and PFHxS (median, 1.6 ng/mL) were detected in 100% of samples. On average, girls born to mothers with prenatal concentrations of PFOS in the upper tertile weighed 140 g less [95% confidence interval (CI): -238, -42] at birth than girls born to mothers with concentrations in the lower tertile in adjusted models. Similar patterns were seen for PFOA (-133 g; 95% CI: -237, -30) and PFHxS (-108 g; 95% CI: -206, -10). At 20 months, however, girls born to mothers with prenatal concentrations of PFOS in the upper tertile weighed 580 g more (95% CI: 301, 858) when compared with those in the lower tertile. No differences in weight were found for PFOA and PFHxS. CONCLUSIONS: Girls with higher prenatal exposure to each of the PFCs examined were smaller at birth than those with lower exposure. In addition, those with higher exposure to PFOS were larger at 20 months.

Exposure to polyfluoroalkyl chemicals during pregnancy is not associated with offspring age at menarche in a contemporary British cohort.

INTRODUCTION: Polyfluoroalkyl chemicals (PFCs) are commercially synthesized chemicals used in consumer products. Exposure to certain PFCs is widespread, and some PFCs may act as endocrine disruptors. We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC) in the United Kingdom to conduct a nested case-control study examining the association between age at menarche, and exposure to PFCs during pregnancy. METHODS: Cases were selected from female offspring in the ALSPAC who reported menarche before the age of 11.5 years (n = 218), and controls were a random sample of remaining girls (n = 230). Serum samples taken from the girls' mothers during pregnancy (1991-1992) were analyzed using on-line solid-phase extraction coupled to isotope dilution high-performance liquid chromatography-tandem mass spectrometry for 8 PFCs. Logistic regression was used to determine association between maternal serum PFC concentrations, and odds of earlier age at menarche. RESULTS: PFOS and PFOA were the predominant PFCs (median serum concentrations of 19.8 ng/mL and 3.7 ng/mL). All but one PFC were detectable in most samples. Total PFC concentration varied by number of births (inverse association with birth order; p-value < 0.0001) and race of the child (higher among whites; p-value = 0.03). The serum concentrations of carboxylates were associated with increased odds of earlier age at menarche; concentrations of perfluorooctane sulfonamide, the sulfonamide esters and sulfonates were all associated with decreased odds of earlier age at menarche. However, all confidence intervals included the null value of 1.0. CONCLUSIONS: ALSPAC study participants had nearly ubiquitous exposure to most PFCs examined, but PFC exposure did not appear to be associated with altered age at menarche of their offspring.

Trends in hospitalization for empyema in Alaska Native children younger than 10 years of age.

We analyzed hospitalizations for empyema among Alaska Native (AN) children and the general population of US children <10 years of age during the years 1998 to 2007. We also analyzed invasive pneumococcal disease in AN children. Between 1998 and 2000, the average annual hospitalization rate for empyema was higher for AN children (51.8 per 100,000/yr) than that for US children (24.2 [95% confidence interval: 20.4, 27.9] per 100,000/yr), and had increased in 2004-2007 in both populations (59.6 and 36.0 [95% confidence interval: 30.1, 41.8], respectively). Pneumococcal empyema increased in AN children despite a decrease in invasive pneumococcal disease pneumonia.

Role of prenatal characteristics and early growth on pubertal attainment of British girls.

OBJECTIVES: The objective of this study was to explore the influence of maternal prenatal characteristics and behaviors and of weight and BMI gain during early childhood on the timing of various puberty outcomes in girls who were enrolled in the Avon Longitudinal Study of Parents and Children. METHODS: Repeated self-assessments of pubertal development were obtained from approximately 4000 girls between the ages of 8 and 14. Data on prenatal characteristics and weight at birth and 2, 9, and 20 months of age were obtained from questionnaires, birth records, and clinic visits. Infants' weights were converted to weight-for-age and BMI SD scores (SDSs; z scores), and change values were obtained for the 0- to 20-month and other intervals within that age range. We used parametric survival models to estimate associations with age of entry into Tanner stages of breast and pubic hair and menarche. RESULTS: Maternal initiation of menarche at age<12, smoking during pregnancy, and primiparity were associated with earlier puberty. A 1-unit increase in the weight SDS change values for the 0- to 20-month age interval was associated with earlier ages of entry into pubertal outcomes (0.19-0.31 years). Increases in the BMI SDS change values were also associated with earlier entry into pubertal outcomes (0.07-0.11 years). CONCLUSIONS: Many of the maternal prenatal characteristics and weight and BMI gain during infancy seemed to have similar influences across different puberty outcomes. Either such early factors have comparable influences on each of the hormonal processes involved in puberty, or processes are linked and awakening of 1 aspect triggers the others.

Pubertal pathways in girls enrolled in a contemporary british cohort.

Data from the Avon Longitudinal Study of Parents and Children were used to describe initiation of secondary sexual characteristic development of girls. Tanner stages of breast and pubic hair and menarche status were self-reported via mailed questionnaires, administered from ages 8-14. Initiation pathway was categorized as breast [thelarche] or pubic hair [pubarche] development alone, or synchronous. Average ages at beginning breast and pubic hair development were estimated using survival analysis. Factors associated with initiation pathway were assessed using logistic regression. Among the 3938 participants, the median ages at beginning breast and pubic hair development were 10.19 (95% CI: 10.14-10.24) and 10.95 (95% CI: 10.90-11.00) years. Synchronous initiation was the most commonly reported pathway (46.3%), followed by thelarche (42.1%). Girls in the pubarche pathway were less likely to be obese or overweight at age 8 or have an overweight or obese mother. Girls in the thelarche pathway were less likely to be of nonwhite race or be the third born or later child.

Characterization of the correlation between ages at entry into breast and pubic hair development.

PURPOSE: The timing of breast and pubic hair development in girls are related, but the degree of correlation has not been well characterized. Periodic observations also are complicated by interval censoring. METHODS: Data used were from the Avon Longitudinal Study of Parents and Children. Mean age at entry into breast and pubic hair development was determined by the use of parametric survival analysis. The bivariate normal cumulative distribution function was evaluated over the region containing the paired event times; the likelihood was maximized with respect to the correlation coefficient rho. RESULTS: Among 3938 participants, estimated mean ages at entry into Tanner stage 2 for breast and pubic hair development were 10.19 and 10.95, respectively. The likelihood was maximized at rho = 0.503 to 0.506. This value remained relatively constant among subgroups, although some heterogeneity was observed by maternal and child body mass index and birth order. CONCLUSIONS: The timing of breast and of pubic hair development is moderately correlated and remain so when it is stratified by characteristics associated with puberty.