ABSTRACT
An exhaustive search of the literature on the growth of mold on fiberglass insulation materials was conducted. Because of the paucity of published material, both peer-reviewed and non-peer-reviewed articles were included. The literature indicates that fiberglass can serve as a support matrix for the collection of debris which, when moist, have the capability of supporting the growth of mold. Further, binding and paper-based moisture barriers from fiberglass resins are also capable of supporting the growth of mold when moist.
Subject(s)
Air Pollution, Indoor , Construction Materials , Fungi/growth & development , Glass , WaterABSTRACT
A deletion polymorphism for glutathione S-transferase M1 (GSTM1) has been related to risk for lung cancer among smokers in some studies but not in others. We examined GSTM1, a GSTT1 deletion polymorphism and a common GSTP1 gene variant (iso-->val), as risk factors for lung cancer in a population-based case-control study of men. Cases (N=274) were males identified from 1993 to 1996 through the Fred Hutchinson Cancer Research Center Cancer Surveillance System registry for western Washington State. Male age-matched controls (N=501) were selected by random-digit dialing. Subjects participated in a telephone interview and blood draw. GSTM1 and GSTT1 were genotyped with a multiplex PCR assay using beta-globin as a positive control, and GSTP1 single nucleotide variant determined with PCR-based oligonucleotide ligation assays. GSTM1 absence was associated with a modest elevation in risk among all cases (odds ratio=1.27, 95% CI 0.91-1.77) and among non-small cell cancers (adenocarcinoma OR=1.58, 95% CI 0.99-2.52; squamous cell OR=1.40, 95% CI 0.83-2.34). Risk associated with GSTM1 null was increased two to sixfold among heavy smokers. GSTT1 was not associated with lung cancer risk and GSTP1 val was non-significantly associated with a modest reduction in risk, particularly among heavy smokers. No specific combination of GST genotypes was particularly associated with risk. These results support previous reports that the GSTM1 null genotype is associated with a modest increase in risk for lung cancer, particularly among heavy smokers, suggest no role for GSTT1 and the need for further study of GSTP1.