Chronic Exposures to Cholinesteraseinhibiting Pesticides Adversely Affect RespiratoryHealth of Agricultural Workers in India: Sreeparna CHAKRABORTY, et al. Department of Experimental Hematology, Chittaranjan National Cancer Institute, India-Objective: The impact of long term exposure to cholinesterase (ChE)-inhibiting organophosphate (OP) and carbamate (C) pesticides on the respiratory health of agricultural workers in India was investigated. Methods: Three hundred and seventy-six nonsmoking agricultural workers (median age 41 yr) from eastern India who sprayed OP and C pesticides in the field and 348 age-and sex-matched control subjects with non-agricultural occupations from the same locality were enrolled. Prevalence of respiratory symptoms was obtained by questionnaire survey, and pulmonary function tests were carried out by spirometry. Chronic obstructive pulmonary disease (COPD) was diagnosed by the Global Obstructive Lung Disease (GOLD) criteria, and erythrocyte acetylcholinesterase (AChE) was measured by the Ellman method. Results: Agricultural workers had greater prevalences of upper and lower respiratory symptoms, and appreciable reduction in spirometric measurements. Overall, lung function reduction was noted in 48.9% of agricultural workers compared with 22.7% of control, and a restrictive type of deficit was predominant. COPD was diagnosed in 10.9% of agricultural workers compared with 3.4% of controls (p<0.05 in χ 2 test), and the severity of the disease was greater in agricultural workers. Red blood cell (RBC) AChE was lowered by 34.2% in agricultural workers, and the fall in AChE level was positively associated with respiratory symptoms, lung function decrement and COPD after controlling for education and income as potential confounders. Conclusions: Long-term exposure to cholinesteraseinhibiting agricultural pesticides currently in use in India is associated with a reduction in lung function, COPD and a rise in respiratory symptoms. (J Occup Health 2009; 51: 488-497)

No abstract

The majority of households in rural India still rely on unprocessed solid biomass for domestic energy. The aim of this study was to investigate whether chronic exposure to biomass smoke causes activation of leukocytes and the formation of leukocyte-platelet aggregates. We conducted flow cytometric analysis of β2 Mac-1 integrin (CD11b/CD18) expression on polymorphonuclear leukocytes (PMN) and monocytes, and P-selectin (CD62P) expression on the platelets of 165 women from eastern India, who cook solely with wood, dung and agricultural wastes, and 155 age- and socio-economic condition-matched control subjects, who used relatively cleaner fuel, liquefied petroleum gas (LPG). Leukocyte-platelet aggregates were defined as CD11b-positive PMN and monocytes co-expressing platelet-specific markers CD41 or CD62P. A significant increase in leukocyte-platelet aggregates was found in women who used biomass as cooking fuel. In addition, they showed increased surface expression of CD11b/CD18 in circulating PMN and monocytes and CD62P expression on platelets. The mean fluorescence intensity (MFI) of CD11b on the surface of circulating monocytes and PMN of biomass users increased by 50 and 68%, respectively. Similarly, a 62 and 48% increase in MFI was observed in CD18 expression on the surface of these cells in biomass users. The results show that chronic biomass smoke exposure activates circulating platelets, PMN and monocytes, and increases the number of leukocyte-platelet aggregates, which are considered a risk factor for thrombosis.

Plasma Catecholamine Levels and Neurobehavioral Problems in Indian Firefighters: Manas R. RAY, et al. Experimental Hematology Unit, Chittaranjan National Cancer Institute, IndiaFirefighting is a stressful and hazardous job. Persons engaged in firefighting are highly exposed to workrelated stress as well as to smoke containing a host of chemicals potentially harmful to human health. In order to elucidate whether firefighting affects neuroendocrine and behavioral responses of firefighters, plasma catecholamine (CA) levels and the prevalence of neurobehavioral symptoms in 62 firefighters (all males, mean age 43 yr) and 52 control subjects matched for age and sex were examined in this study. Self-reported neurobehavioral symptoms data were obtained from a questionnaire survey and personal interview. Concentrations of epinephrine (E), norepinephrine (NE) and dopamine (DA) in plasma were measured by highp e r f o r m a n c e l i q u i d c h r o m a t o g r a p h y w i t h electrochemical detection. Compared with matched controls, the firefighters showed higher prevalence (p<0.05) of neurobehavioral symptoms such as burning sensation in the extremities, tingling and numbness, transient loss of memory, and depression, but no significant difference was recorded in the prevalences of anxiety, vertigo and dizziness. The firefighters demonstrated a more than two-fold (p<0.05) rise in plasma levels of E and NE, but the plasma DA level was relatively unchanged. Controlling age and smoking as possible confounders, firefighting was found to be associated with raised E (OR=2.15; 95% CI, 0.98-4.52), and NE levels (OR=2.24 95% CI, 1.22-3.61).In conclusion, the job of firefighting appears to be associated with stimulation of sympathetic activity and a rise in the prevalence of neurobehavioral symptoms. (J Occup Health 2006; 48: 210-215)

No abstract

Benzene exposure from vehicular sources and its health impact are relatively unexplored in India. We have investigated in this study hematology and lymphocyte subsets of 25 petrol pump attendants, 25 automobile service station workers and 35 controls matched for age, sex and socioeconomic conditions. The participants were non-smoking males of Kolkata (former Calcutta) in eastern India. Compared with controls, the workers had 3.8- times more trans,trans-muconic acid in urine, suggesting higher level of benzene exposure. The exposed subjects had decreased erythrocyte, hemoglobin, lymphocyte and platelet levels, but increased neutrophil, band cells, RBC aniso-poikilocytosis and target cells. In addition, CD4+, CD8+ and CD19+ cells were decreased by 37, 20 and 47% respectively, but CD 16+ 56+ NK cells were increased by 20%. P-selectin expression on platelet surface of the workers was significantly elevated (P < 0.05), indicating upregulation of platelet activity. In summary, the study revealed high level of benzene exposure from vehicular sources in India, and the exposed subjects had hematological and immunological alterations.

This study examined whether indoor air pollution from biomass fuel burning induces DNA damage in airway cells. For this, sputum cells were collected from 56 premenopausal rural women who cooked with biomass (wood, dung, crop residues) and 49 age-matched controls who cooked with cleaner liquefied petroleum gas. The levels of particulate matters with diameters of less than 10 and 2.5 µm (PM(10) and PM(2.5)) in indoor air were measured using a real-time aerosol monitor. Benzene exposure was monitored by measuring trans,trans-muconic acid (t,t-MA) in urine by HPLC-UV. DNA damage was examined by alkaline comet assay in sputum cells. Generation of reactive oxygen species (ROS) and level of superoxide dismutase (SOD) in sputum cells were measured by flow cytometry and spectrophotometry, respectively. Compared with controls, biomass users had 4 times higher tail percentage DNA, 37% more comet tail length and 5 times more Olive tail moment (p < 0.001) in inflammatory and epithelial cells in sputum, suggesting extensive DNA damage. In addition, women who cooked with biomass had 6 times higher levels of urinary t,t-MA and 2-fold higher levels of ROS generation concomitant with 28% depletion of SOD. Indoor air of biomass-using households had 2-4 times more PM(10) and PM(2.5) than that of controls. After controlling potential confounders, positive association was found between DNA damage parameters, particulate pollution, urinary t,t-MA and ROS. Thus, long-term exposure to biomass smoke induces DNA damage in airway cells and the effect was probably mediated, at least in part, by oxidative stress generated by inhaled particulate matter and benzene.

Cumulative exposure to biomass smoke causes lung function decrement and facilitates COPD development even in non-smoking and relatively young pre-menopausal women.