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1.  Clinical investigation of an outbreak of alveolitis and asthma in a car engine manufacturing plant 
Thorax  2007;62(11):981-990.
Exposure to metal working fluid (MWF) has been associated with outbreaks of extrinsic allergic alveolitis (EAA) in the USA, with bacterial contamination of MWF being a possible cause, but is uncommon in the UK. Twelve workers developed EAA in a car engine manufacturing plant in the UK, presenting clinically between December 2003 and May 2004. This paper reports the subsequent epidemiological investigation of the whole workforce. The study had three aims: (1) to measure the extent of the outbreak by identifying other workers who may have developed EAA or other work‐related respiratory diseases; (2) to provide case detection so that those affected could be treated; and (3) to provide epidemiological data to identify the cause of the outbreak.
The outbreak was investigated in a three‐phase cross‐sectional survey of the workforce. In phase I a respiratory screening questionnaire was completed by 808/836 workers (96.7%) in May 2004. In phase II 481 employees with at least one respiratory symptom on screening and 50 asymptomatic controls were invited for investigation at the factory in June 2004. This included a questionnaire, spirometry and clinical opinion. 454/481 (94.4%) responded and 48/50 (96%) controls. Workers were identified who needed further investigation and serial measurements of peak expiratory flow (PEF). In phase III 162 employees were seen at the Birmingham Occupational Lung Disease clinic. 198 employees returned PEF records, including 141 of the 162 who attended for clinical investigation. Case definitions for diagnoses were agreed.
87 workers (10.4% of the workforce) met case definitions for occupational lung disease, comprising EAA (n = 19), occupational asthma (n = 74) and humidifier fever (n = 7). 12 workers had more than one diagnosis. The peak onset of work‐related breathlessness was Spring 2003. The proportion of workers affected was higher for those using MWF from a large sump (27.3%) than for those working all over the manufacturing area (7.9%) (OR = 4.39, p<0.001). Two workers had positive specific provocation tests to the used but not the unused MWF solution.
Extensive investigation of the outbreak of EAA detected a large number of affected workers, not only with EAA but also occupational asthma. This is the largest reported outbreak in Europe. Mist from used MWF is the likely cause. In workplaces using MWF there is a need to carry out risk assessments, to monitor and maintain fluid quality, to control mist and to carry out respiratory health surveillance.
PMCID: PMC2117138  PMID: 17504818
2.  Occupational exposure to environmental tobacco smoke and health risk assessment. 
Environmental Health Perspectives  1999;107(Suppl 6):829-835.
This article addresses concepts of environmental tobacco smoke (ETS) exposure assessment relevant for health risk assessment based on human studies. We present issues that should be considered when selecting a method for ETS exposure assessment for the purposes of health risk assessment and review data on ETS exposure levels in the workplace and in home environments. Two types of estimates are needed for a quantitative risk assessment of the health effects resulting from occupational ETS exposure: (italic)a(/italic)) an unbiased estimate of the exposure-effect (or dose-response) relation between ETS and the health effect of interest, and (italic)b(/italic)) estimates of the distribution of ETS exposure in different workplaces. By combining the estimated exposure-effect relation with information on exposure distribution for a population of interest, we can calculate the proportions of disease cases attributable to occupational ETS exposure as well as the excess number of cases due to specified exposure conditions. Several dimensions of the exposure profile should be considered when assessing ETS exposure for estimating the exposure-effect relation, including the magnitude of exposure and the biologically relevant time specificity of exposure. The magnitude of exposure is determined by the ETS source strength, environmental factors modifying concentrations, and duration of exposure. Time specificity considerations include the latency period for each health outcome of interest, the time-exposure profile relevant for different disease mechanisms, and the sensitive age period with regard to health effects. The most appropriate indicator of ETS exposure depends on these factors and on the time period that can be assessed with different methods.
PMCID: PMC1566195  PMID: 10592138
3.  Summary: workshop on health risks attributable to ETS exposure in the workplace. 
Environmental Health Perspectives  1999;107(Suppl 6):823-828.
This 1998 workshop was convened to address the health risks of exposure to environmental tobacco smoke (ETS) in the workplace. It was paired with a 1997 workshop on issues related to ETS exposure in work environments ((italic)1(/italic)). In the 1998 workshop, a multidisciplinary group of participants was charged with reviewing evidence on the quantitative risks to health posed by ETS and to discuss development of risk assessment methodology for the future. The overall charges for the present workshop were to consider various health outcomes and make recommendations regarding those health outcomes to be included in assessment of health risk resulting from ETS in the workplace; to consider available studies addressing these health outcomes and to evaluate the validity of data for estimating risk from occupational ETS exposure; to review and evaluate mathematical models useful for estimating the risk due to ETS exposure; to examine dose-response models and to characterize the models regarding validity and uncertainty in estimating health risk attributable to ETS exposure in the workplace.
PMCID: PMC1566201  PMID: 10592151
4.  Increased serum pancreatitis associated protein (PAP) concentration after longterm alcohol consumption: further evidence for regular subclinical pancreatic damage after heavy drinking? 
Gut  1995;36(1):117-120.
It has been shown recently that longterm but not short term heavy drinking of alcohol frequently results in increased serum activities of pancreatic enzymes suggesting subclinical pancreatic injury. Serum pancreatitis associated protein (PAP) is a novel protein, whose synthesis in the acinar cells and release into serum is specifically induced by acute pancreatic damage. This study was performed to further characterise the alcohol induced subclinical pancreatic injury by using serum PAP measurements. Three groups were studied: (1) control group (n = 25), (2) short term drinking group (n = 20), who consumed 2.0 g of ethanol per kg body weight during four hours, and (3) longterm drinking group (n = 32), who were admitted to withdrawal clinic after a median 30 months heavy drinking period. Serum PAP concentration was low in the control group (8 (5 to 12) micrograms/l, geometric mean (95% confidence intervals)). In the short term drinking group serum PAP was in the range of the control group values during 56 hours after drinking. Longterm drinking induced at least a 10-fold increase in serum PAP, the highest concentrations being seen on day 2 after drinking had ended (106 (61 to 184) micrograms/l). The patients did not develop abdominal symptoms, increased blood white cell count, or increased serum C reactive protein concentration. These results further support the suggestion that heavy longterm drinking often induces subclinical pancreatic damage, but not clinical pancreatitis.
PMCID: PMC1382364  PMID: 7890213
5.  Effect of cigarette smoking on evolution of ventilatory lung function in young adults: an eight year longitudinal study. 
Thorax  1991;46(12):907-913.
BACKGROUND: There are few data on the quantitative effects of cigarette smoking on lung function in young adults. These effects are important in the understanding of the early stages of chronic airflow obstruction. METHODS: A longitudinal study over eight years was carried out to estimate quantitatively the effect of cigarette smoking on ventilatory lung function in young adults and to examine the possibility that the effect is modified by other factors. The study population were 15 to 40 years of age at initial examination, when they underwent spirometry and completed an interviewer administered questionnaire on respiratory health. Eight years later 391 of the subjects were re-examined (38% response rate). The quantitative effect of cigarette smoking during the study period on the average change of forced expiratory volume in one second (FEV1) over time (delta FEV1) was estimated in two linear regression models that included potential confounders and other determinants of outcome. RESULTS: The first model showed a significant dose-response relation between the average rate of smoking during the study period and delta FEV1, giving an estimate of annual change in FEV1 of -0.42 ml for each cigarette smoked per day (-8.4 ml for each pack) (p = 0.04). In the second model, which took smoking before the study period as a potential confounder, the effect of smoking during the study period was slightly smaller (-0.33 ml/year for each cigarette smoked per day). This indicated that smoking before the study period had a marginal latent effect on delta FEV1 during the study. However, neither the effect of smoking before the study nor that of smoking during the study was significant, presumably because of collinearity. Interactions between cigarette smoking and gender, wheezing, atopy, and exposure to environmental tobacco smoke during the growth period were not significant with respect to their effect on the relation between cigarette smoking and delta FEV1. CONCLUSION: Cigarette smoking has a dose related adverse effect on the evolution of ventilatory lung function in young adulthood.
PMCID: PMC463497  PMID: 1792639
6.  Pancreatitis in Finland between 1970 and 1989. 
Gut  1993;34(9):1255-1260.
The incidence and mortality from pancreatitis in Finland between 1970 and 1989 were studied and compared with the alcohol consumption in the country and with the incidence of liver cirrhosis and gall stone disease. Hospital discharge data were obtained from the Finnish National Agency for Welfare and Health, the causes of deaths from the Finnish State Statistics, and annual alcohol consumption from the Finnish State Alcohol Company. There were 56,353 hospital treatment periods because of pancreatitis. The incidence of pancreatitis discharges increased from 46.6 to 73.4/100,000/year. In men it increased from 59.1 to 113.4, but in women it remained unchanged (mean 35.0). The incidence of pancreatitis discharges correlated with the alcohol consumption in Finland (r = 0.78, p = 0.0001). The incidence of pancreatitis discharges correlated in men, but not in women, with the incidence of liver cirrhosis (r = 0.81, p = 0.0001). In women, but not in men, the incidence of pancreatitis discharges correlated with the incidence of gall stone disease discharges (r = 0.77, p = 0.0001). The incidence of discharges due to haemorrhagic pancreatitis and pancreatic abscess doubled in men and remained unchanged in women. Pancreatitis death rate decreased from 5.9% (men 4.8%, women 7.0%) to 2.6% (men 2.4%, women 2.7%).
PMCID: PMC1375465  PMID: 8406164

Results 1-6 (6)