Results of the present study substantiate that occupational exposure to TCE causes respiratory ailments, which
is evident by the decline of pulmonary function. TCE exposure also reduces body fat%. The study also supports the
association between TCE exposure and disturbances in cell
cycle regulation, which is indicated by increasing expression levels of p53, p21 and bax mRNAs together with
decreasing levels of bcl-2 mRNA. Nonetheless, involvement
of DHEAS as an endogenous ligand of PPARA is uncertain
in the observed changes in the levels of various mRNAs.
However, the significant decrease in the DHEAS level of the
exposed workers in comparison to the controls indicates its
potential for endocrine disruption. Further, no difference
was observed in PPARA mRNA and let-7c miRNA expression in exposed workers. Further studies are essential to
explore the entire mechanism of TCE toxicity by attempting
additional human studies.