{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:37:21Z","timestamp":1787017041799,"version":"build-2736575974"},"reference-count":30,"publisher":"BMJ","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Occup Environ Med"],"published-print":{"date-parts":[[2007,6]]},"abstract":"<jats:p>\n                    <jats:bold>Objectives:<\/jats:bold>\n                    Endotoxin exposure induces airway inflammation, hyper-responsiveness and higher expression of tumour necrosis factor (TNF). This study was conducted to investigate whether\n                    <jats:italic>TNF<\/jats:italic>\n                    polymorphisms modify the effect of endotoxin exposure on chronic declines in lung function.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:<\/jats:bold>\n                    Associations between\n                    <jats:italic>TNF<\/jats:italic>\n                    and\n                    <jats:italic>LTA<\/jats:italic>\n                    polymorphisms, endotoxin exposure and lung function were analysed in 263 cotton workers and 230 silk workers as a reference group, who were prospectively followed for 20 years. Multiple linear regression models were used to assess the association, with adjustment for smoking and other covariates.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    Endotoxin exposure was associated with faster lung function decline among genotypes associated with higher TNF expression levels, with estimates of annual FEV\n                    <jats:sub>1<\/jats:sub>\n                    change in relation to endotoxin exposure of \u20132.9 ml and \u20136.8 ml in the\n                    <jats:italic>G\/G<\/jats:italic>\n                    and\n                    <jats:italic>G\/A+AA<\/jats:italic>\n                    genotypes, respectively, for the\n                    <jats:italic>TNF<\/jats:italic>\n                    polymorphism; and \u20132.0 ml, \u20134.0 ml and \u20133.6 ml in\n                    <jats:italic>A\/A<\/jats:italic>\n                    ,\n                    <jats:italic>A\/G<\/jats:italic>\n                    and\n                    <jats:italic>G\/G<\/jats:italic>\n                    genotypes, respectively, for the\n                    <jats:italic>LTA<\/jats:italic>\n                    polymorphism. When joint effects of endotoxin exposure and smoking were considered, the effect modification of\n                    <jats:italic>TNF<\/jats:italic>\n                    and\n                    <jats:italic>LTA<\/jats:italic>\n                    polymorphisms was prominent in never smokers.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusions:<\/jats:bold>\n                    <jats:italic>TNF<\/jats:italic>\n                    and\n                    <jats:italic>LTA<\/jats:italic>\n                    polymorphisms may modify the association between occupational endotoxin exposure and longitudinal lung function decline, which was more clearly observed in never smokers.\n                  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