Bidisha Mukherjee

Hypertension with elevated levels of oxidized low-density lipoprotein and anticardiolipin antibody in the circulation of premenopausal Indian women chronically exposed to biomass smoke during cooking.

UNLABELLED This study aims to investigate whether indoor air pollution (IAP) from biomass fuel use was associated with hypertension, platelet hyperactivity, and elevated levels of oxidized low-density lipoprotein (oxLDL) and anticardiolipin antibody (aCL). We enrolled 244 biomass fuel-using (median age 34 year) and 236 age-matched control women who cooked with liquefied petroleum gas (LPG). Enzyme-linked immunosorbent assay was used to measure oxLDL in plasma and aCL in serum, flow cytometry for P-selectin expression on platelet and reactive oxygen species (ROS) generation by leukocytes, aggregometry for platelet aggregation, spectrophotometry for superoxide dismutase (SOD) in erythrocytes, and laser photometer for particulate matter <10 and 2.5 μm in diameter (PM(10) and PM(2.5), respectively) in cooking areas. Biomass users had three times more particulate pollution in kitchen, had higher prevalence of hypertension (29.5 vs. 11.0% in control, P < 0.05), elevated oxLDL (170.6 vs. 45.9 U/l; P < 0.001), platelet P-selectin expression (9.1% vs. 2.4%), platelet aggregation (23.2 vs. 15.9 Ohm), raised aCL IgG (28.7% vs. 2.1%), IgM (8.6% of vs. 0.4%), and ROS (44%) but depleted (13%) SOD. After controlling potential confounders, the changes were positively associated with PM(10) and PM(2.5) in indoor air, suggesting a positive association between IAP and increased cardiovascular risk. PRACTICAL IMPLICATIONS The study showing high risk of developing cardiovascular diseases (CVD) among poor, underprivileged women in their reproductive ages in rural India is important from public health perspectives. It may motivate the government and the regulatory agencies of the country to take a serious note of the indoor air pollution (IAP) from biomass fuel use as it threatens the health of millions of women, children, and the elderly who mostly stay indoor. We hope the findings will strengthen the demand for setting up a standard for indoor air quality in the country in the line of national ambient air quality standard. The findings may also inspire the authorities to take measures for the reduction in IAP by improving housing, kitchen ventilation, and cook stoves. Moreover, the parameters used in this study can be utilized for large, population-based studies to identify women at a higher risk of developing CVD so that medical intervention can be taken at the formative stage of a disease.

Micronucleus formation, DNA damage and repair in premenopausal women chronically exposed to high level of indoor air pollution from biomass fuel use in rural India

Genotoxicity of indoor air pollution from biomass fuel use has been examined in 132 biomass users (median age 34 years) and 85 age-matched control women from eastern India who used the cleaner fuel liquefied petroleum gas (LPG) to cook. Micronucleus (MN) frequency was evaluated in buccal (BEC) and airway epithelial cells (AEC); DNA damage was examined by comet assay in peripheral blood lymphocytes (PBL); and expressions of gamma-H2AX, Mre11 and Ku70 proteins were localized in AEC and PBL by immunocytochemistry. Reactive oxygen species (ROS) generation in leukocytes was measured by flow cytometry, and the levels of superoxide dismutase (SOD) and total antioxidant status (TAS) in blood were measured by spectrophotometry. Real-time aerosol monitor was used to measure particulate pollutants in indoor air. Compared with controls, biomass users had increased frequencies of micronucleated cells in BEC (3.5 vs. 1.7, p<0.001) and AEC (4.54 vs. 1.86, p<0.001), and greater comet tail % DNA (18.6 vs. 11.7%, p<0.01), tail length (45.5 vs. 31.4mum, p<0.01) and olive tail moment (4.0 vs. 1.4, p<0.01) in PBL. Moreover, biomass users had more gamma-H2AX-positive nuclei in PBL (49.5 vs. 8.5%, p<0.01) and AEC (11.3 vs. 2.9%, p<0.01) along with higher expression of DNA repair proteins Mre11 and Ku70 in these cells, suggesting stimulation of DNA repair mechanism. Biomass users showed rise in ROS generation and depletion of SOD and TAS. Biomass-using households had 2-4 times more particulate matter with diameter less than 10 and 2.5mum in indoor air, and MN frequency and comet tail % DNA were positively associated with these pollutants after controlling potential confounders. Thus, chronic exposure to biomass smoke causes chromosomal and DNA damage and upregulation of DNA repair mechanism.

Chronic inhalation of biomass smoke is associated with DNA damage in airway cells: involvement of particulate pollutants and benzene.

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 (PM10 and PM2.5) 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 PM10 and PM2.5 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. Copyright

Platelet hyperactivity, neurobehavioral symptoms and depression among Indian women chronically exposed to low level of arsenic

The prevalence of neurobehavioral symptoms (NBS) and depression has been investigated in premenopausal rural women of West Bengal, India enrolled from arsenic (As) endemic (groundwater As 11-50 μg/L; n = 342) and control areas (As level ≤ 10 μg/L; n = 312). The subjective symptoms questionnaire and Becks 21-point depression inventory-II were used for the detection of NBS and depression, respectively. Platelet P-selectin expression was measured by flow cytometry, plasma neurotransmitter activity with high performance liquid chromatography and groundwater As level by atomic absorption spectroscopy. The As level in groundwater was 2.72 ± 1.18 μg/L in control and 28.3 ± 13.51 μg/L in endemic areas (p < 0.0001). Women residing in endemic areas demonstrated a higher prevalence of depressive symptoms (39.8 vs. 19.9%, p < 0.001) and anxiety (43.3 vs. 18.0% in control, p < 0.001), fatigue (68.4 vs. 23.4%, p < 0.0001), reduced sense of taste (15.8 vs. 4.5%, p<0.0001) and smell (14.9 vs. 5.8%, p < 0.001); burning sensation (36.8 vs. 5.4%, p < 0.0001) and tingling or numbness in the extremities (25.1 vs. 5.1%, p < 0.0001); and transient loss of memory (69.9 vs. 28.2%, p < 0.001). As-exposed women had 1.6-times more plasma epinephrine and norepinephrine (p < 0.05), 1.8-times higher level plasma serotonin with 28.9% lower intraplatelet serotonin (p < 0.05 for both), but their plasma dopamine level was not significantly different (p>0.05) from that of controls. Moreover, women from endemic areas had 2.3-times more P-selectin-expressing platelets in their circulation (p < 0.001). After controlling the potential confounders, chronic low level As (11-50 μg/L) exposure showed a positive association with the prevalence of neurobehavioral symptoms and depression among Indian women in their child-bearing age.

Indoor Air Pollution from Biomass Burning Activates Akt in Airway Cells and Peripheral Blood Lymphocytes A Study among Premenopausal Women in Rural India

Biomass burning is a major source of indoor air pollution in rural India. The authors investigated in this study whether cumulative exposures to biomass smoke cause activation of the serine/threonine kinase Akt in airway cells and peripheral blood lymphocytes (PBL). For this, the authors enrolled 87 premenopausal (median age 34 years), nonsmoking women who used to cook with biomass (wood, dung, crop wastes) and 85 age-matched control women who cooked with cleaner fuel liquefied petroleum gas. Immunocytochemical and immunoblotting assays revealed significantly higher levels of phosphorylated forms of Akt protein (p-Aktser473 and p-Aktthr308) in PBL, airway epithelial cells, alveolar macrophages, and neutrophils in sputum of biomass-using women than control. Akt activation in biomass users was associated with marked rise in generation of reactive oxygen species and concomitant depletion of superoxide dismutase. Measurement of particulate matter having a diameter of less than 10 and 2.5 µm in indoor air by real-time aerosol monitor showed 2 to 4 times more particulate pollution in biomass-using households, and Akt activation was positively associated with particulate pollution after controlling potential confounders. The findings suggest that chronic exposure to biomass smoke activates Akt, possibly via generation of oxidative stress.

Chronic Low Level Arsenic Exposure Inflicts Pulmonary and Systemic Inflammation

Objective: To examine whether chronic low level arsenic (As) exposure (11-50 µg/L) from drinking water elicits inflammation and oxidative stress. Methods: Never-smoking pre-menopausal women (n=267) from Nadia district, West Bengal, India, were enrolled into two groups (i) control (n=122, median age 39 yr) from villages with <10 µg/L of As in groundwater, and (ii) exposed (n=145, median age 38 yr) from the same district where the groundwater As was 11-50 µg/L. As in water was measured by atomic absorption spectrophtometry with vapour generation assembly. Sputum cytology and hematology were done by standard procedures. Enzyme-linked immunosorbent assays were used to measure tumor necrosis factor-alpha (TNF-α), interleukin-6, 8, 10, 12 (IL-6, IL-8, IL-10, IL-12) and C-reactive protein (CRP) in plasma and cortisol in serum. Serum nitric oxide (NO) was measured colorimetrically, myleperoxidase (MPO) and neutrophil elastase by spectrophotometry, reactive oxygen species (ROS) by flow cytometry, and inducible nitric oxide synthase (iNOS) by immunocytochemistry. Results: As level in groundwater was higher in endemic areas (28.32 ± 13.51 vs. 2.72 ± 1.18, p<0.05), and exposed women had lower hemoglobin, leukocyte and erythrocyte levels but elevated platelet count than control and their sputum contained increased number of alveolar macrophages and inflammatory cells. In addition, they had elevated levels of TNF-α, IL-8, IL-6, IL-12, CRP, cortisol and NO but depleted level of IL-10 with excess generation of ROS and increased expression of iNOS in the airways. Neutrophils of As-exposed subjects had elevated levels of MPO and elastase. After controlling education and family income as potential confounders, the rise in pro-inflammatory mediators in blood and excess generation of ROS in the airways were positively associated with As levels in ground water. Conclusion: Drinking of water contaminated with low level of As for long causes pulmonary and systemic inflammation and generates excess ROS in the airways.

Estimation of detergent influx and impact assessment in freshwaters

Abstract An equation is derived which rigorously defines the partitioning of inorganic carbon flux into alkali addition, calcium precipitation, production and respiration in fresh waters, polluted by the influx of detergents. The model has been extended to account for the modulation of oxygen concentration due to the oxygen demand of detergents (ODD). The equation is applied to two such polluted systems receiving detergent influx in the range of 50–285 g m −3 (as calcium carbonate equivalent). The flux in the various parameters has been compared with unpolluted systems and with laboratory simulation studies, to assess the impact of detergents. Given certain assumptions, the influx can be visualized in the form of an environmental stress, reducing productivity. The degree of reduction varies with the loading of the system.

Increased oxidative DNA damage and decreased expression of base excision repair proteins in airway epithelial cells of women who cook with biomass fuels

To investigate whether biomass burning causes oxidative DNA damage and alters the expression of DNA base excision repair (BER) proteins in airway cells, sputum samples were collected from 80 premenopausal rural biomass-users and 70 age-matched control women who cooked with liquefied petroleum gas. Compared with control the airway cells of biomass-users showed increased DNA damage in alkaline comet assay. Biomass-users showed higher percentage of cells expressing oxidative DNA damage marker 8-oxoguanine and lower percentages of BER proteins OGG1 and APE1 by immunocytochemical staining. Reactive oxygen species (ROS) generation was doubled and level of superoxide dismutase was depleted significantly among biomass-users. The concentrations of particulate matters were higher in biomass-using households which positively correlated with ROS generation and negatively with BER proteins expressions. ROS generation was positively correlated with 8-oxoguanine and negatively with BER proteins suggesting cooking with biomass is a risk for genotoxicity among rural women in their child-bearing age.

Increased cardiovascular risk in association with chronic airflow obstruction among premenopausal rural women of India who cook exclusively with biomass

We aimed to compare the cardiovascular risk in biomass-using women with or without chronic obstructive pulmonary disease (COPD). A total of 22 biomass-using married women with COPD and 24 matched controls with normal lung function were enrolled for this purpose. Platelet P-selectin (P-sel) expression and platelet–leukocyte aggregation were determined using flow cytometry. Platelet aggregation by collagen was measured by aggregometer. Soluble P-selectin (sP-sel), tumor necrosis factor-alpha (TNF-α), interleukin-8, -6, -10 (IL-8, IL-6, IL-10), neutrophil-activating protein-2 (NAP-2), C-reactive protein (CRP), oxidized low density lipoprotein (oxLDL) in plasma were measured by enzyme-linked immunosorbent assay. Generation of reactive oxygen species (ROS) by leukocytes was measured by flow cytometry, and erythrocyte content of superoxide dismutase (SOD) was measured by spectrophotometry. Particulate matter with a diameter of less than 2.5 μm (PM2.5) in indoor air was measured by real-time aerosol monitor. Compared with control, biomass users with COPD had increased expression of platelet P-selectin, elevated levels of sP-sel, oxLDL, TNF-α, IL-8, IL-6, NAP-2, CRP, lowered IL-10 and more circulating platelet-neutrophil (p < 0.0001) and platelet–monocyte (p < 0.0001) aggregates. ROS generation was increased by 19.5% while SOD was depleted by 32% in women with COPD. Biomass smoke-induced COPD is associated with excess cardiovascular risk via oxidative stress, platelet activation, and inflammation.