Description: Introduction Reductions in heavy manual work as a consequence of mechanisation might adversely impact muscle strength at older ages. We investigated the association between grip strength at retirement age and lifetime occupational exposure to physically demanding activities. Grip strength is an important predictor of long-term health and physical function in older people. Methods Grip strength (maximum of three readings in each hand) was measured in men from the Hertfordshire Cohort Study at a single examination when their mean age was 65.8 (SD 2.9) years. Associations with lifetime occupational exposure (ascertained by questionnaire) to three activities (standing/walking ≥4 h/day; lifting ≥25 kg; and energetic work sufficient to induce sweating) were assessed by multivariable linear regression with adjustment for various potential confounders. Results Complete data were available from 1418 men who had worked for at least 20 years. After adjustment for age, height and weight, those with longer exposures to walking/standing and heavy lifting had lower grip strength, but the relationship disappeared after further adjustment for confounders. Working at physical intensity sufficient to induce sweating was not significantly associated with grip strength. Conclusions We found no evidence that physically demanding occupational activities increase hand grip strength at normal retirement age. Any advantages of regular physical occupational activity may have been obscured by unmeasured socioeconomic confounders.

Description: Background Welders are at risk for cardiovascular disease. Recent studies linked tobacco smoke exposure to hypomethylation of the F2RL3 (coagulation factor II (thrombin) receptor-like 3) gene, a marker for cardiovascular disease prognosis and mortality. However, whether welding fumes cause hypomethylation of F2RL3 remains unknown. Methods We investigated 101 welders (median span of working as a welder: 7 years) and 127 unexposed controls (non-welders with no obvious exposure to respirable dust at work), age range 23–60 years, all currently non-smoking, in Sweden. The participants were interviewed about their work history, lifestyle factors and diseases. Personal sampling of respirable dust was performed for the welders. DNA methylation of F2RL3 in blood was assessed by pyrosequencing of four CpG sites, CpG_2 (corresponds to cg03636183) to CpG_5, in F2RL3 . Multivariable linear regression analysis was used to assess the association between exposure to welding fumes and F2RL3 methylation. Results Welders had 2.6% lower methylation of CpG_5 than controls (p〈0.001). Higher concentrations of measured respirable dust among the welders were associated with hypomethylation of CpG_2, CpG_4 and CpG_5 (β=–0.49 to –1.4, p〈0.012); p〈0.029 adjusted for age, previous smoking, passive smoking, education, current residence and respirator use. Increasing the number of years working as a welder was associated with hypomethylation of CpG_4 (linear regression analysis, β=–0.11, p=0.039, adjusted for previous smoking). Previous tobacco smokers had 1.5–4.7% (p〈0.014) lower methylation of 3 of the 4 CpG sites in F2RL3 (CpG_2, CpG_4 and CpG_5) compared to never-smokers. A non-significant lower risk of cardiovascular disease with more methylation was observed for all CpG sites. Conclusions Welding fumes exposure and previous smoking were associated with F2RL3 hypomethylation. This finding links low-to-moderate exposure to welding fumes to adverse effects on the cardiovascular system, and suggests a potential mechanistic pathway for this link, via epigenetic effects on F2RL3 expression.

Description: Objectives Animal evidence shows that N -nitrosamines and similar xenobiotic compounds are pancreatic carcinogens. We aimed to determine whether occupational exposure to N- nitrosamines or to pesticides increases risk of pancreatic cancer development. Methods Participants (504 cases, 643 controls) in a population-based case–control study (The Queensland Pancreatic Cancer Study) provided data on demographic, medical and lifestyle factors and lifetime job histories. Specific questions were asked regarding work in rubber and leather industries, metalworking jobs and occupational or direct use of pesticides on animals or crops. An occupational hygienist reviewed this information (blind to case status) to assess likelihood of exposure to N- nitrosamines and pesticides, and estimated level and frequency of such exposures. Results No associations were found for risk of pancreatic cancer and occupational exposure to N- nitrosamines (OR=0.85, 95% CI 0.51 to 1.42) and no associations were seen with level or frequency of exposure. No associations were observed for ever exposure to pesticides in general (OR=0.90, 95% CI 0.61 to 1.33) or to any of the pesticide subgroups. Stratification by history of cigarette smoking did not change these results. Conclusions This comprehensive analysis of a large case–control study does not support an association between occupational exposure to N- nitrosamines or pesticide use and risk of pancreatic cancer.

Description: Objectives Previous experimental and epidemiological research suggests that maternal exposure to some organic solvents during pregnancy may increase the risk of fetal growth restriction (FGR). We evaluated the association between expert-assessed occupational solvent exposure and risk of small for gestational age (SGA) infants in a population-based sample of women in the National Birth Defects Prevention Study. Methods We analysed data from 2886 mothers and their infants born between 1997 and 2002. Job histories were self-reported. Probability of exposure to six chlorinated, three aromatic and one petroleum solvent was assessed by industrial hygienists. SGA was defined as birthweight〈10th centile of birthweight-by-gestational age in a national reference. Logistic regression was used to estimate ORs and 95% CIs to assess the association between SGA and exposure to any solvent(s) or specific solvent classes, adjusting for maternal age and education. Results Approximately 8% of infants were SGA. Exposure prevalence to any solvent was 10% and 8% among mothers of SGA and non-SGA infants, respectively. Among women with ≥50% probability of exposure, we observed elevated but imprecise associations between SGA and exposure to any solvent(s) (1.71; 0.86 to 3.40), chlorinated solvents (1.70; 0.69 to 4.01) and aromatic solvents (1.87; 0.78 to 4.50). Conclusions This is the first population-based study in the USA to investigate the potential association between FGR and assessed maternal occupational exposure to distinct classes of organic solvents during pregnancy. The potential associations observed between SGA and exposure to chlorinated and aromatic solvents are based on small numbers and merit further investigation.

Description: Objectives Although the serum granulocyte-macrophage colony stimulating factor autoantibody (GMAb) levels have been recognised as a diagnostic marker in primary pulmonary alveolar proteinosis (PAP), their role in PAP with occupational inhalational exposure (PAPo) remains unclear. Methods Forty-five consecutive patients with PAP were enrolled. Each patient with PAP was assessed for baseline clinical characteristics, chest high-resolution CT (HRCT), serum GMAb and occupational exposure. Fifty healthy controls were included to define normal ranges for GMAb levels. Ninety-seven hospital controls with other respiratory diseases were included to establish prevalence of a history of occupational inhalation exposure. Results According to the serum GMAb cut-off value of 2.39 μg/mL, 84.4% of the recruited patients with PAP had positive serum GMAb with a median level of 28.7 μg/mL, defined as autoimmune PAP, and the remaining 15.6% had negative serum GMAb with a median level of 0.16 μg/mL, defined as non-autoimmune PAP. Also, 34.2% of patients with autoimmune PAP had a history of occupational inhalational exposure, which was not significantly higher than that of hospital controls (34.2% vs 19.6%, p=0.072). Four patients with PAPo showed negative GMAb. Their arterial oxygen tension, pulmonary function parameters and chest HRCT features were significantly different when compared with patients with autoimmune PAP (p〈0.05). These four non-autoimmune occupational lung disease cases culminated in 3 deaths and a lung transplant. Conclusions A number of patients with PAP who may have occupational inhalational exposure and negative serum GMAb represent a high possibility of silicoproteinosis and very poor survival.

Description: Occupational exposures have been shown to be risk factors for chronic obstructive pulmonary disease (COPD) among never-smokers. In a Danish population-based cohort, we analysed this association and the population attributable fraction. The study population (N=1575) was aged 45–84, COPD was defined by lung function measurements and the method of lower limit of normal (LLN), and occupational exposure was assessed by questionnaire and expert judgement. Furthermore, the estimates additionally were provided according to the Global Initiative for Chronic Obstructive Lung Diseases. More than a threefold increased risk (LLN OR=3.69 (95% CI 1.36 to 10.04) was found for occupational exposure to vapour, gas, dust and fumes (predominantly organic dust) in this never-smoking population, with a corresponding 48% (95% CI 30% to 65%) population attributable fraction among never-smokers.

Description: Objectives We investigated the association between six occupational exposures (ie, pesticides, solvents, metals, diesel motor emissions (DME), extremely low frequency magnetic fields (ELF-MF) and electric shocks) and Parkinson's disease (PD) mortality in a large population-based prospective cohort study. Methods The Netherlands Cohort Study on diet and cancer enrolled 58 279 men and 62 573 women aged 55–69 years in 1986. Participants were followed up for cause-specific mortality over 17.3 years, until December 2003, resulting in 402 male and 207 female PD deaths. Following a case–cohort design, a subcohort of 5 000 participants was randomly sampled from the complete cohort. Information on occupational history and potential confounders was collected at baseline. Job-exposure matrices were applied to assign occupational exposures. Associations with PD mortality were evaluated using Cox regression. Results Among men, elevated HRs were observed for exposure to pesticides (eg, ever high exposed, HR 1.27, 95% CI 0.86 to 1.88) and ever high exposed to ELF-MF (HR 1.54, 95% CI 1.00 to 2.36). No association with exposure duration or trend in cumulative exposure was observed for any of the occupational exposures. Results among women were unstable due to small numbers of high-exposed women. Conclusions Associations with PD mortality were observed for occupational exposure to pesticides and ELF-MF. However, the weight given to these findings is limited by the absence of a monotonic trend with either duration or cumulative exposure. No associations were found between PD mortality and occupational exposure to solvents, metals, DME or electric shocks.

Description: Objective To compare short-term effects of fine particles (PM 2.5 ; aerodynamic diameter 〈2.5 µm) from different sources on the blood levels of markers of systemic inflammation. Methods We followed a panel of 52 ischaemic heart disease patients from 15 November 2005 to 21 April 2006 with clinic visits in every second week in the city of Kotka, Finland, and determined nine inflammatory markers from blood samples. In addition, we monitored outdoor air pollution at a fixed site during the study period and conducted a source apportionment of PM 2.5 using the Environmental Protection Agency's model EPA PMF 3.0. We then analysed associations between levels of source-specific PM 2.5 and markers of systemic inflammation using linear mixed models. Results We identified five source categories: regional and long-range transport (LRT), traffic, biomass combustion, sea salt, and pulp industry. We found most evidence for the relation of air pollution and inflammation in LRT, traffic and biomass combustion; the most relevant inflammation markers were C-reactive protein, interleukin-12 and myeloperoxidase. Sea salt was not positively associated with any of the inflammatory markers. Conclusions Results suggest that PM 2.5 from several sources, such as biomass combustion and traffic, are promoters of systemic inflammation, a risk factor for cardiovascular diseases.

Description: Pesticides, including herbicides, insecticides, fungicides, fumigants and rodenticides, provide important benefits in public health, food production and aesthetics ( http://www.epa.gov/agriculture/ag101/pestbenefits.html ). Unlike most other important chemicals, pesticides are designed to impact living systems ( http://www.cdc.gov/niosh/docs/81-123/ ). Consequently there has long been a concern about environmental and human consequences of widespread pesticide use. Carson 1 effectively voiced this concern and documented some problems in her 1962 book, Silent Spring. Global pesticide use increased dramatically between the 1960s and 1990s, and more slowly thereafter, but large increases continue to occur in many developing countries. 2 The estimated worldwide use in 2007 was 5211 million pounds of active ingredients, with herbicides accounting for the major use in agriculture, and about 40% of the use overall. 3 To place this figure in context, it is close to one pound for each of the 6.6 billion people then inhabiting the globe, albeit...

Description: Objectives The role of outdoor air pollution in the incidence of chronic obstructive pulmonary disease (COPD) remains unclear. We investigated this question using a large, nationally representative cohort based on primary care records linked to hospital admissions. Methods A cohort of 812 063 patients aged 40–89 years registered with 205 English general practices in 2002 without a COPD diagnosis was followed from 2003 to 2007. First COPD diagnoses recorded either by a general practitioner (GP) or on admission to hospital were identified. Annual average concentrations in 2002 for particulate matter with an aerodynamic diameter 〈10 µm (PM 10 ) and 〈2.5 µm (PM 2.5 ), nitrogen dioxide (NO 2 ), ozone and sulfur dioxide (SO 2 ) at 1 km 2 resolution were estimated from emission-based dispersion models. Hazard ratios (HRs) per interquartile range change were estimated from Cox models adjusting for age, sex, smoking, body mass index and area-level deprivation. Results 16 034 participants (1.92%) received a COPD diagnosis from their GP and 2910 participants (0.35%) were admitted to hospital for COPD. After adjustment, HRs for GP recorded COPD and PM 10 , PM 2.5 and NO 2 were close to unity, positive for SO 2 (HR=1.07 (95% CI 1.03 to 1.11) per 2.2 µg/m 3 ) and negative for ozone (HR=0.94 (0.89 to 1.00) per 3 µg/m 3 ). For admissions HRs for PM 2.5 and NO 2 remained positive (HRs=1.05 (0.98 to 1.13) and 1.06 (0.98 to 1.15) per 1.9 µg/m 3 and 10.7 µg/m 3 , respectively). Conclusions This large population-based cohort study found limited, inconclusive evidence for associations between air pollution and COPD incidence. Further work, utilising improved estimates of air pollution over time and enhanced socioeconomic indicators, is required to clarify the association between air pollution and COPD incidence.