ABSTRACT
Background: Occupational exposure to polycyclic aromatic hydrocarbons (PAHs) has been shown to be associated with lung cancer in various epidemiological studies in industries such as aluminium reduction/smelting, coal gasification, coke production, iron/steel foundries, coal/coke and related products and carbon/graphite electrodes production. Aims: To update data on the association between PAH exposure and morbidity and mortality due to lung cancer among workers in different occupations, including smoking data. Methods: A comprehensive literature search was conducted to retrieve relevant papers for meta-analysis. Cohort studies with standardized mortality ratios or standardized incidence ratios and calculated overall risk ratio with their corresponding 95% confidence intervals (CIs) were included in the analysis. Chi-square test for heterogeneity was used to evaluate the consistency of findings between the studies. Results: A significant risk of lung cancer was observed among the coal/coke and related product industry 1.55 (95% CI 1.01-2.37) and the iron/steel foundry industry 1.52 (95% CI 1.05-2.20). There was a wide variation in smoking habits and PAHs exposure among studies. Conclusions: Coal/coke industry and iron/steel industry workers showed a higher risk of lung cancer compared with other occupations exposed to PAHs. The confounding effects of smoking and individual exposure levels of PAH should be taken into account.
Subject(s)
Lung Neoplasms/etiology , Manufacturing Industry , Occupational Exposure/adverse effects , Polycyclic Aromatic Hydrocarbons/adverse effects , Chi-Square Distribution , Humans , Incidence , Lung Neoplasms/epidemiology , Manufacturing Industry/methods , Manufacturing Industry/statistics & numerical data , Occupational Exposure/statistics & numerical dataABSTRACT
An important role of oxidative stress for the development of vascular and neurological complications has encouraged us to undertake a study to assess the oxidative stress induced nerve conduction deficits among cigarette smokers. Eighteen regular male cigarette smokers and twenty nine male non-smokers were diagnosed for clinical neuro-physiological tests viz., motor and sensory nerve conduction velocity (MNCV and SNCV) and redox status. Significant depletion of reduced glutathione (GSH) level (p < 0.05) and significant increase in malondialdehyde (MDA) level (p < 0.01) was found in smokers compared to non-smokers. Motor and sensory nerve conduction velocity showed no significant difference among smokers compared to non-smokers. The present study shows that smoking can induce oxidative stress among smokers but could not exacerbate to nerve conduction deficits.
