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Page 10 of 16                                               Burke. Plast Aesthet Res 2020;7:59  I  http://dx.doi.org/10.20517/2347-9264.2020.154








































               Figure 4. The aryl hydrocarbon receptor (AHR). The AHR is found in the cytoplasm bound to protein chaperone molecules, including
               AHR interacting protein, heat shock protein-90, the p53 protein, and the tyrosine kinase oncogene cSRC. When a pollutant ligand
               binds to this complex, conformational changes dissemble the complex so that the ligand-AHR unit translocates into the nucleus
               where it dimerizes with ARNT. The ligand-AHR-ARNT entity induces transcription of target genes, specific for each xenobiotic ligand.
               Overstimulation by the ligand-AHR complex is prevented (1) by RNA transcription of the AHR repressor (AHRR) gene to synthesize co-
               repressors; and (2) by cytoplasmic degradation of the ligand-AHR entity after expulsion from the nucleus. After release from the initial
               cytoplasmic AHR complex, the chaperone protein oncogene cSRC binds to the epidermal growth factor receptor (EGFR), activating the
               cSRC protein kinase to induce carcinogenesis. (Modified from Figure 1 of Vogeley et al. [47]  with the author’s consent.). cSRC: “cellular
               sarcoma”, photo oncogene tyrosine-protein kinase; ARNT: AHR nuclear translocator


               increase in pollution measured. Concentrated soot increased lentigines by 27% on the forehead and 20% on
               the cheeks. Women living within 100 m of a busy road showed an increase of 25% and 20% in forehead and
               cheeks lentigines, respectively, for each interquartile increase in pollution.

                                                                                                       [49]
               A further study looked at the VOC NO  released by traffic, known to cause lung damage and lung cancer .
                                                2
               Facial cheek lentigines were evaluated in women over 50 years old - 806 European Caucasians and 1,072
               Chinese, making this the largest study to date of traffic-induced lentigines. Indeed, NO  exposure increased
                                                                                         2
               lentigines in both cohorts. Lentigines develop at a younger age in Asians despite their cultural avoidance
               of sun exposure (in contrast to many Caucasians). This proclivity for lentigines may be due to a particular
               genetic marker in the SLC45A2 gene similarly noted in Japanese, a marker known to be involved in
                              [50]
               melanin synthesis .

               Indoor pollution
               Cigarette smoke is the most significant indoor contaminant; second-hand side-stream smoke permeates
               indoor space and is recycled in closed environment; third-hand smoke is carried by the hair, skin, and
                                                    [40]
               clothes of smokers entering a closed space . In 1969, Henry Daniell recognized that smokers look older
               than non-smokers . Several epidemiological papers confirm this observation [52,53,54] . Analysis shows that
                               [51]
               men who smoke have 2.3 times as many wrinkles as nonsmoking males, and women have 3.1 times as
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