Page 51 - Biennial Report 2018-20 Jun 2021
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international standards, but normal by Indian standards, are much more likely to have clinically
                  significant elevation of IL8 or TNF-α, as compared to those who are normal by international
                  standards. Shorter and  thinner children showed poorest z scores for lung function, after
                  accounting for height, weight, and gender, suggestive of nutritional stunting being important
                  along with possible gut dysbiosis as a cause of the low grade chronic inflammation. Data from
                  the Pune Birth Cohort suggested protein intake to be a potential factor and the early life head
                  circumference/length ratio to be an inverse predictor.

                  Biochemical parameters were estimated for additional 1000 subjects. The trends obtained by
                  reanalyzing data including the new data points were consistent with the previous findings. These
                  results confirm the negative association between inflammatory cytokines (IL8, TNF-α) and lung
                  function, adjusted for all other relevant parameters. A positive association was also observed
                  between haemoglobin levels and lung function.


                  DIESEL EXHAUST AND ITS IMPACT ON RESPIRATORY HEALTH



                  Diesel exhaust has proved to be major contributor of urban air pollution contributing 28% of the
                  PM. Therefore, the group led by Naveen Arora is studying molecular aspect of diesel exhaust
                  exposure (DEE) on lung health and disease phenotype associated with its exposure.
                  Present analysis of the murine model of diesel exhaust exposure has shown decremental effect
                  on lung health. DEE significantly increases total and differential cell count (macrophages, mono-
                  nuclear and neutrophil) compared to control. Accumulation of particulate matter and carbon-
                  laden macrophages were seen in the cells. Cytokine analysis showed increased expression of
                  proinflammatory cytokines IL-6 & TNF-α.  IL-17A and TGF-β  (profibrotic)  were  significantly
                  increased in the mice exposed to DE. Lung histology showed thickening of bronchiolar wall and
                  infiltration of  immune cells  in bronchiolar and alveolar region. Relative expression  of genes
                  involved in fibrosis i.e., α-SMA, Fibronectin and MMP-9 was significantly increased in lung tissue.
                  TGF-β  downstream  signaling  genes  like  smad  3,  smad  4  and  snail  1  were  also  significantly
                  increased. miRNA profiling illustrated 30 differentially expressed miRNA, of which miR-145, miR-
                  29c and miR-30e were involved in tissue fibrosis. Future studies will involve in deciphering the
                  pathways involved in lung fibrosis along with oxidative & antioxidant imbalance involved in diesel
                  exhaust exposure.



                  SOLID WASTE DUMPING SITES AS CAUSE OF AIR POLLUTION AND CONSEQUENT
                  RESPIRATORY HEALTH RISKS


                  Studies on traffic policemen and in health camps for people living near solid waste dump sites
                  and engaged in occupation of waste disposal have shown surprising results. While pollution
                  levels on roads and at these sites are very high, there are no clear correlates with lung function.
                  Traffic policemen had better lung function than control subjects at all ages and showed lower
                  decline. This may be because of better health at the time of selection into the police. Locals living
                  near the dump for longer periods had better lung  function than recent immigrants. Socio-
                  economic and other health determinants seem to be stronger predictors of lung function than
                  air pollution of gaseous or solid types.
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