Higher Beetle Diversity in Native Vegetation Than in Stands of the Invasive Arundo, Arundo donax L., along the Rio Grande Basin in Texas, USA.

Within the cattle fever tick quarantine zone along the Rio Grande, a steady displacement of native vegetation by Arundo donax L. has been occurring for over a century. Arundo rapidly grows to a height of 3-6 m creating a dense wall of vegetation impeding surveillance and interception of stray cattle breaching the cattle fever tick quarantine from Mexico. Additionally, arundo monocultures may decrease the number and diversity of predatory beetles feeding on cattle fever ticks. To compare predatory beetle abundance and diversity within and between arundo and native vegetation, beetles were trapped at 10 locations twice a month for 16 mo (=38,400 trap nights) in the cattle fever tick quarantine zone along the Mexico-American border between Brownsville and Del Rio, TX. In total, 766 beetles were trapped, which included 34 genera and 43 species. Native vegetation provided more beetles, greater species richness, and increased biological diversity. Thus, greater beetle diversity was found in the more complex native vegetation compared with arundo stands. However, because predatory beetle sample numbers were modest, it is unlikely these mostly polyphagous, opportunistic arthropod predators would apply much pressure on tick populations, leading us to conclude that beetle predation would have little effect on tick populations in native vegetation or within stands of arundo.

Impaired OMA1-dependent cleavage of OPA1 and reduced DRP1 fission activity combine to prevent mitophagy in cells that are dependent on oxidative phosphorylation.

Mitochondrial dynamics play crucial roles in mitophagy-based mitochondrial quality control, but how these pathways are regulated to meet cellular energy demands remains obscure. Using non-transformed human RPE1 cells, we report that upregulation of mitochondrial oxidative phosphorylation alters mitochondrial dynamics to inhibit Parkin-mediated mitophagy. Despite the basal mitophagy rates remaining stable upon the switch to dependence on oxidative phosphorylation, mitochondria resist fragmentation when RPE1 cells are treated with the protonophore carbonyl cyanide m-chlorophenyl hydrazone. Mechanistically, we show that this is because cleavage of the inner membrane fusion factor L-OPA1 is prevented due to the failure to activate the inner membrane protease OMA1 in mitochondria that have a collapsed membrane potential. In parallel, mitochondria that use oxidative phosphorylation are protected from damage-induced fission through the impaired recruitment and activation of mitochondrial DRP1. Using OMA1-deficient MEF cells, we show that the preservation of a stable pool of L-OPA1 at the inner mitochondrial membrane is sufficient to delay mitophagy, even in the presence of Parkin. The capacity of cells that are dependent on oxidative phosphorylation to maintain substantial mitochondrial content in the face of acute damage has important implications for mitochondrial quality control in vivo.

Resolution of inter and intra-species relationships of the West Indian fruit fly Anastrepha obliqua.

The West Indian fruit fly, Anastrepha obliqua (Diptera: Tephritidae), is an economically important pest that inhabits areas of South and Central America, Mexico and the Caribbean with occasional infestations in the southern United States. We examine intra-specific relationships within A. obliqua as well as interspecific relationships to other Anastrepha species using a multi-locus data set comprising nine loci (seven nuclear, two mitochondrial) with 105 operational taxonomic units. The results based on a concatenated set of nuclear loci strongly support the monophyly of A. obliqua and most of the other species previously identified by morphology. A split between Peruvian A. obliqua samples and those from other locations was also identified. These results contrast with prior findings of relationships within A. obliqua based on mitochondrial data, as we found a marked discrepancy between nuclear and mitochondrial loci. These analyses suggest that introgression, particularly between A. obliqua and fraterculus species, may be one explanation for the discrepancy and the high mitochondrial diversity reported for A. obliqua could be the result of incomplete lineage sorting.

Glucagon increases energy expenditure independently of brown adipose tissue activation in humans.

AIMS: To investigate, for a given energy expenditure (EE) rise, the differential effects of glucagon infusion and cold exposure on brown adipose tissue (BAT) activation in humans. METHODS: Indirect calorimetry and supraclavicular thermography was performed in 11 healthy male volunteers before and after: cold exposure; glucagon infusion (at 23 °C); and vehicle infusion (at 23 °C). All volunteers underwent (18)F-fluorodeoxyglucose ((18)F-FDG) positron emission tomography (PET)/CT scanning with cold exposure. Subjects with cold-induced BAT activation on (18)F-FDG PET/CT (n = 8) underwent a randomly allocated second (18)F-FDG PET/CT scan (at 23 °C), either with glucagon infusion (n = 4) or vehicle infusion (n = 4). RESULTS: We observed that EE increased by 14% after cold exposure and by 15% after glucagon infusion (50 ng/kg/min; p < 0.05 vs control for both). Cold exposure produced an increase in neck temperature (+0.44 °C; p < 0.001 vs control), but glucagon infusion did not alter neck temperature. In subjects with a cold-induced increase in the metabolic activity of supraclavicular BAT on (18)F-FDG PET/CT, a significant rise in the metabolic activity of BAT after glucagon infusion was not detected. Cold exposure increased sympathetic activation, as measured by circulating norepinephrine levels, but glucagon infusion did not. CONCLUSIONS: Glucagon increases EE by a similar magnitude compared with cold activation, but independently of BAT thermogenesis. This finding is of importance for the development of safe treatments for obesity through upregulation of EE.

Targeted siRNA Screens Identify ER-to-Mitochondrial Calcium Exchange in Autophagy and Mitophagy Responses in RPE1 Cells.

Autophagy is an important stress response pathway responsible for the removal and recycling of damaged or redundant cytosolic constituents. Mitochondrial damage triggers selective mitochondrial autophagy (mitophagy), mediated by a variety of response factors including the Pink1/Parkin system. Using human retinal pigment epithelial cells stably expressing autophagy and mitophagy reporters, we have conducted parallel screens of regulators of endoplasmic reticulum (ER) and mitochondrial morphology and function contributing to starvation-induced autophagy and damage-induced mitophagy. These screens identified the ER chaperone and Ca2+ flux modulator, sigma non-opioid intracellular receptor 1 (SIGMAR1), as a regulator of autophagosome expansion during starvation. Screens also identified phosphatidyl ethanolamine methyl transferase (PEMT) and the IP3-receptors (IP3Rs) as mediators of Parkin-induced mitophagy. Further experiments suggested that IP3R-mediated transfer of Ca2+ from the ER lumen to the mitochondrial matrix via the mitochondrial Ca2+ uniporter (MCU) primes mitochondria for mitophagy. Importantly, recruitment of Parkin to damaged mitochondria did not require IP3R-mediated ER-to-mitochondrial Ca2+ transfer, but mitochondrial clustering downstream of Parkin recruitment was impaired, suggesting involvement of regulators of mitochondrial dynamics and/or transport. Our data suggest that Ca2+ flux between ER and mitochondria at presumed ER/mitochondrial contact sites is needed both for starvation-induced autophagy and for Parkin-mediated mitophagy, further highlighting the importance of inter-organellar communication for effective cellular homeostasis.

Possible pro-carcinogenic association of endotoxin on lung cancer among Shanghai women textile workers.

BACKGROUND: Endotoxin (lipopolysaccharide) is a widespread contaminant in many environmental settings. Since the 1970s, there has been generally consistent evidence indicating reduced risks for lung cancer associated with occupational endotoxin exposure. METHODS: We updated a case-cohort study nested within a cohort of 267,400 female textile workers in Shanghai, China. We compared exposure histories of 1456 incident lung cancers cases diagnosed during 1989-2006 with those of a reference subcohort of 3022 workers who were free of lung cancer at the end of follow-up. We applied Cox proportional hazards modelling to estimate exposure-response trends, adjusted for age and smoking, for cumulative exposures lagged by 0, 10, and 20 years, and separately for time windows of ⩽15 and >15 years since first exposure. RESULTS: We observed no associations between cumulative exposure and lung cancer, irrespective of lag interval. In contrast, analyses by exposure time windows revealed modestly elevated, but not statistically significant relative risks (∼1.27) at the highest three exposure quintiles for exposures that occurred >15 years since first exposure. CONCLUSIONS: The findings do not support a protective effect of endotoxin, but are suggestive of possible lung cancer promotion with increasing time since first exposure.

Catastrophic antiphospholipid syndrome with concurrent thrombotic and hemorrhagic manifestations.

Antiphospholipid syndrome (APS) is a distinct autoimmune prothrombotic disorder due to pathogenic autoantibodies directed against proteins that bind to phospholipids. APS is characterized by arterial and venous thrombosis and their clinical sequelae. Catastrophic antiphospholipid syndrome (CAPS) is a rare and often fatal form of APS characterized by disseminated intravascular thrombosis and ischemic injury resulting in multiorgan failure. Rarely, intravascular thrombosis in CAPS is accompanied by hemorrhagic manifestations such as diffuse alveolar hemorrhage. Here, we report a 43-year-old woman who presented with anemia, acute gastroenteritis, abnormal liver function tests, bilateral pulmonary infiltrates, and a systemic inflammatory response syndrome. The patient developed respiratory failure as a result of diffuse alveolar hemorrhage followed by acute renal failure. Laboratory tests disclosed hematuria, proteinuria, and reduced platelet count. Microbiologic tests were negative. A renal biopsy demonstrated acute thrombotic microangiopathy and extensive interstitial hemorrhage. Serologic tests disclosed antinuclear antibodies and reduced serum complement C4 concentration. Coagulation studies revealed the lupus anticoagulant and autoantibodies against cardiolipin, beta 2-glycoprotein I, and prothrombin. High-dose glucocorticoids and plasma exchange resulted in rapid resolution of pulmonary, renal, and hematological manifestations. This rare case emphasizes that CAPS can present with concurrent thrombotic and hemorrhagic manifestations. Rapid diagnosis and treatment may result in complete recovery.

Lung cancer and occupational exposures other than cotton dust and endotoxin among women textile workers in Shanghai, China.

OBJECTIVES: Numerous epidemiological studies of lung cancer among textile workers worldwide consistently indicate reduced risks related to cotton dust exposure, presumably due to endotoxin contamination. Our objective was to investigate associations with other exposures potentially related to lung cancer, including wool and synthetic fibre dusts, formaldehyde, silica, dyes and metals, that have only been studied to a limited extent in the textile industry. METHODS: We conducted a case-cohort study nested within a cohort of 267,400 women textile workers in Shanghai, China. We compared work assignments and exposure histories of 628 incident lung cancer cases, diagnosed during 1989-1998, with those of a reference subcohort of 3188 workers. We reconstructed exposures with a job-exposure matrix developed specifically for textile factories. Cox proportional hazards modelling was applied to estimate age/smoking-adjusted relative risks (hazard ratios) and risk gradients associated with job assignments and specific agents other than cotton dust and endotoxin. RESULTS: No associations were observed for lung cancer with wool, silk or synthetic fibre dusts, or with most other agents. However, increased risks, although statistically imprecise, were noted for ≥ 10 years' exposures to silica (adjusted HR 3.5, 95% CI 1.0 to 13) and ≥ 10 years' exposures to formaldehyde (adjusted HR 2.1, 95% CI 0.4 to 11). CONCLUSIONS: Exposures to silica and formaldehyde, although not widespread among the cohort, may have increased lung cancer risk. Silica is an established human lung carcinogen, whereas there is only weak prior evidence supporting an association with formaldehyde. Both exposures warrant consideration as potential lung carcinogens in textile manufacturing.

Membrane antigens specific for human lymphoid cells in the dividing phase.

Heteroantisera were raised in rabbits against human thymocytes or Burkitt's lymphoma EBI cells. After suitable absorption, the sera were specific for thymocytes and T lymphoblasts, or B lymphoblasts and several lymphoblastoid cell lines. The specificity of the antisera was confirmed by preparing purified populations of T or B lymphocytes on immunoabsorbent columns, followed by mitogenic stimulation with phytohemagglutinin. The antisera did not react with normal resting lymphocytes.

A regulatory role for the memory B cell as suppressor-inducer of feedback control.

A regulatory role is proposed for the antigen-responsive B cell, as suppressor-inducer of feedback control during the secondary response in vivo. In a double adoptive transfer of memory cells primed to a thymus-dependent antigen from one irradiated host to another, antigen-specific suppressors are generated after a critical time in the primary recipient, able to entirely ablate a secondary anti-hapten response. Positive cell selection in the fluorescence-activated cell sorter confirmed that suppression was mediated by an Lyt-2+ T cell; however, positively selected B cells were also inhibitory and able to induce suppressors in a carrier-specific manner: Bhapten induced suppressors in a carrier-primed population, and Bcarrier induced suppressors in a hapten-carrier population. At the peak of the antibody response in the primary host, memory B cells and their progeny were unable to differentiate further to plasma cells due to their intrinsic suppressor-inducer activity, but this autoregulatory circuit could be severed by adoptive transfer to carrier-primed, X-irradiated recipients.

Modulation of immunodominant sites in influenza hemagglutinin compromise antigenic variation and select receptor-binding variant viruses.

The regions of antigenic variation in influenza hemagglutinin (HA) are located on surface-accessible regions in the three-dimensional structure of the HA1 monomer. The aim of this study was to establish whether a novel variant virus, IMUT4, in which we had mutated specific amino acid residues (HA1 63, 144, 158, and 193) in these regions, previously shown to be immunodominant for CBA/Ca mice, would either (a) establish holes in the antibody (ab) repertoire or (b) preclude further antigenic variation in IMUT4. CBA/Ca mice were able to mount a neutralizing ab response to IMUT4 infection and molecular recognition sites were established by sequencing of the HA genes of monoclonal antibody (mAb)-selected laboratory variants of wild-type X31 virus (HA1 131, 145, 155, and 196). However, each of these mAbs failed to select further antigenic variants of IMUT4, in ovo, but rather a receptor binding mutant (HA1 190 Glu-->Asp; 226 Leu-->Gln) that was still recognized by the selecting mAb, specific for HA1 155 of X31 virus. The facility for antigenic variation in influenza would appear to be compromised, therefore, by targeted mutation of immunodominant sites, as initially proposed by S. Fazekas de St. Groth (Fazekas de St. Groth, S. 1977. Antigenic, adaptive and adsorptive variants of the influenza haemagglutinin. In Topics in Infectious Diseases. Vol. 3. R.G. Laver, H. Bachmayer, and R. Weil, editors. Springer-Verlag, Vienna. 25-48.). It is interesting to note that recent isolates of the H3 subtype, (e.g., A/Beijing/92) obtained between 1991 and 1993, contain the same substitutions at HA1 190 and 226, which may indicate similar constraints to immune evasion and the relevance of our findings to antigenic variation in the human population.

Extensive diversity in the recognition of influenza virus hemagglutinin by murine T helper clones.

A panel of H-2k class II-restricted Th clones were established from individual CBA mice primed by infection with X31 influenza virus. 27 clones, which showed specific recognition of the HA surface glycoprotein, were all H3N2 subtype specific, in contrast to a T cell line which was crossreactive and which may have other specificities. 20 distinct HA-specific clones recognized a tryptic cleavage fragment of X31 consisting of residue 28-328 of HA1 (tops) which includes all the Ab-combining regions of the HA molecule. Seven other HA-specific clones failed to respond to either tops or to aggregate (the remainder of the virus after tryptic cleavage of tops). The specificity of these clones has been mapped, tentatively, to a conformational determinant in the interface antibody-binding region of the HA trimer. Analysis of the fine specificity of the HA-specific clones against a panel of H3N2 natural variant viruses isolated from major virus epidemics from 1968 to 1984 revealed a hitherto unrecognized diversity in T cell recognition of a HA. A total of 12 specificity groupings were evident, and varied from groups of clones that recognized all natural variants to one clone that responded only to isolates from 1968 to 1972. Six out of eight clones from a major specificity group, which failed to recognize variants TX/77, BK/79, or CN/84, responded to two overlapping peptides (48-68 and 53-87), corresponding to a region of HA1 that includes part of two antibody combining sites. An examination of the amino acid sequences of natural variant viruses from this region of HA revealed that residues Asn53 and Asn54 and/or Ile62 were critical for recognition by these clones. We conclude that recognition of HA by Th cells is not restricted to a limited number of epitopes in the conserved regions of the molecule, but is extremely diverse and includes specificities that map to variable antibody-combining regions of the molecule. In addition, the sensitivity of the T cell clones to the amino acid substitutions occurring in HA1 of natural variant viruses suggests that Th may play a role in the immune pressure for antigenic variation in the HA molecule.

Diversity of the class II (I-Ak/I-Ek)-restricted T cell repertoire for influenza hemagglutinin and antigenic drift. Six nonoverlapping epitopes on the HA1 subunit are defined by synthetic peptides.

H-2k-restricted T cell clones derived from CBA mice infected with X31 (H3N2) influenza virus, were shown to recognize distinct, nonoverlapping sequences within the HA1 subunit of the viral hemagglutinin (HA) using synthetic peptides. Three I-Ak-restricted T cell sequences were identified within HA1 68-83, 120-139, and 269-288, and two recognition sites presented in the context of the I-Ek molecule were mapped to HA1 sequences 226-245 and 246-265. T cell clones specific for these regions of HA1 demonstrated varying abilities to differentiate between natural variant viruses that had accumulated substitutions within their HA molecules as a result of antigenic drift. Clones that recognized sequences HA1 226-245 and HA1 246-265 failed to discriminate between natural variants and focused on conserved sequences within these epitopes. A majority of T cell clones were sensitive to amino acid substitutions that have featured in antigenic drift occurring within three major antigenic sites of the HA1 subunit; substitutions at HA1 residues 78 (V)/83(K) and 275(D)/278(I) within the HA1 subunit of mutant viruses correlated with a 75% reduction in the proliferative response for T cell clones specific for sequences HA1 68-83 and HA1 269-288, respectively. Furthermore, a clone that recognized HA1 120-139 was nonresponsive to a mutant virus HK/71, implicating amino acids at HA1 position 129(G) and/or 132(Q) within this sequence as crucial for recognition. Our data, together with the previous finding that sequence HA1 53-63 is also a major I-Ak-restricted T cell recognition site, demonstrate a level of diversity in the T cell recognition of influenza HA, within a single mouse haplotype hitherto unrecognized, and imply that the T cell repertoire diversity against foreign antigens may be greater than previously assumed. Furthermore, the frequency at which HA-specific T cells have been identified that focus on amino acids within the HA1 subunit of HA also featuring in antigenic drift, suggests that a failure of MHC class II-restricted T cells to recognize specific epitopes within mutant HA molecules may contribute significantly to the capacity of variant influenza viruses to evade immune recognition.

Structural assignment of novel and immunodominant antigenic sites in the neutralizing antibody response of CBA/Ca mice to influenza hemagglutinin.

Information on the antigenic structure of influenza hemagglutinin (HA) has been deduced previously from sequence analyses of laboratory mutant viruses selected, in vitro, with neutralizing monoclonal antibody (mAb) established exclusively from BALB/c (H-2d) mice; and there has been no attempt to investigate the influence of host genetic background, or natural route of infection, on the protective antibody repertoire. CBA/Ca mice are extremely sensitive to X31 virus infection, and in the present study a structural analysis was made of the antibody repertoire, by direct sequencing of the HA genes of laboratory mutant viruses selected, in ovo with mAb from CBA/Ca mice primed by natural infection with X31 virus at two different infectious doses. Single nucleotide substitutions in the HA genes of mutant viruses identified both novel and immunodominant antigenic sites on the HA1 subunit: a majority of mAbs, from different donors, were of the IgG2a isotype and were specific for HA1 158 Gly. In addition, novel laboratory mutants were obtained containing substitutions in the HA1 subunit that had not been reported previously for H3 subtype viruses, either natural variants or laboratory mutants, at residues: HA1 62 Ile----Arg; HA1 165 Asn----Ser (resulting in the loss of a N-glycosylation site); and HA1 273 Pro----Leu. Our findings suggest that host genetic background and/or a natural route of infection may be significant factors in the selection of different and distinct neutralizing antibody responses to influenza HA and therefore be of some relevance in our further understanding of the immune pressure for antigenic drift, and the immunogenic features of a protective antigen.

Rapid changes in nucleoside transport induced by growth inhibitors. Studies with neoplastic mast cells.

Aqueous extracts of murine embryonic or uterine tissue, or [(6)N]O(2)'-dibutyryl 3',5'-adenosine monophosphate (dbc-AMP) which were cytostatic for the murine mastocytoma P815Y in vitro also induced rapid changes in the incorporation of exogenous nucleosides into acid-insoluble material. However, these alterations were not a consequence of growth arrest. Different dose-response curves were obtained for cytostasis and inhibition of [(3)H]-nucleoside incorporation, and changes in [(3)H]thymidine uptake were detected within 15 min of treatment with the inhibitors. Also, there were differential effects of each inhibitor on the incorporation of (3)H-labeled thymidine, uridine, adenosine, or choline into acid-insoluble material.

Growth inhibition of murine tumor cells, in vitro, by puromycin, ( 6 N)O 2 '-dibutyryl 3',5'-adenosine monophosphate, or adenosine: evidence of commitment for cell division.

The cytostatic effects of puromycm, [(6)N]O(2')-dibutyryl 3',5'-adenosine monophosphate, and adenosine on asynchronous and synchronous cultures of the murine mastocytoma, P815Y, have been studied. Cell growth was arrested after a minimum of one further division. A model is proposed for the inhibition of cell division in which the periods of inhibition and growth arrest are separated in time by one cell cycle.

Dust and chemical exposures, and miscarriage risk among women textile workers in Shanghai, China.

INTRODUCTION: To investigate possible associations between miscarriage and occupational exposures in the Shanghai textile industry. METHODS: A retrospective cohort study of miscarriages among 1752 women in the Shanghai textile industry was conducted. Reproductive history was self-reported by women and occupational work histories were collected from factory personnel records. Occupational exposures were assigned by linking work history information to an industry-specific job-exposure matrix informed by factory-specific textile process information and industrial hygiene assessments. Estimates of cotton dust and endotoxin exposure were also assigned. Odds ratios (OR) and 95% CI were estimated by multivariate logistic regression, with adjustment for age at pregnancy, educational level, smoking status of the woman and her spouse, use of alcohol, and woman's year of birth. RESULTS: An elevation in risk of a spontaneously aborted first pregnancy was associated with exposure to synthetic fibres (OR 1.89, 95% CI 1.20 to 3.00) and mixed synthetic and natural fibres (OR 3.31, 95% CI 1.30 to 8.42). No increased risks were observed for women working with solvents, nor were significant associations observed with quantitative cotton dust or endotoxin exposures. Associations were robust and similar when all pregnancies in a woman's reproductive history were considered. CONCLUSIONS: Occupational exposure to synthetic fibres may cause miscarriages, and this possibility should be the subject of further investigation.

Levels of systemic metal ions in patients with intramedullary nails.

BACKGROUND: It is being increasingly recognized that orthopedic implants are associated with adverse tissue responses, mediated by degradation products. Recent interest has been focused on the production of metal ions from hip arthroplasty. Few studies have reviewed fracture fixation devices and their metal ion production. METHODS: 61 subjects were enlisted into the study, with 3 subgroups. 21 subjects had Russell-Taylor intramedullary tibial nails in situ for 26 (21-32) months (316LVm stainless steel), 20 subjects had TriGen intramedullary tibial nails in situ for 43 (35-51) months (Ti-6Al-4V titanium alloy), and the remaining 20 subjects did not have any implant in situ and served as controls. Blood samples were taken and serum chromium, molybdenum, titanium, aluminium, and vanadium concentrations were measured using inductively coupled plasma (ICP) techniques. RESULTS: The 3 groups were matched for age, sex, and BMI. The subjects with Russell-Taylor nails had elevated levels of chromium (0.10 microg/L) with median concentrations 2.5 times higher than those of the control group. The subjects with TriGen nails had less significantly elevated levels of titanium (6.5 microg/L). INTERPRETATION: Stainless steel implants show significant differences from titanium implants in the dissemination of metal ions. Although the levels of chromium were elevated, the overall levels were modest when compared to published data regarding metal ion release and hip arthroplasty. Intramedullary nails are, however, often used in younger patients. If not removed, they may result in prolonged exposure to metal ions.

Occupational risk factors for nasopharyngeal cancer among female textile workers in Shanghai, China.

AIMS: To investigate whether occupational exposure to dusts and chemicals in the Chinese textile industry are associated with risk of nasopharyngeal cancer. METHODS: Sixty seven nasopharyngeal carcinoma (NPC) cases identified during 1989-98 and a random sample (n = 3188) of women were included in a case cohort study nested in a cohort of 267,400 women textile workers in Shanghai, China. A complete occupational history of work in the textile industry was obtained for each woman. A job exposure matrix developed by experienced industrial hygienists was used to assess exposures to specific dusts and chemicals. RESULTS: Risk of NPC is associated with cumulative exposure to cotton dust. The hazard ratio for women cumulatively exposed to >143.4 mg/m3 x years of cotton dust was 3.6 (95% CI 1.8 to 7.2) compared with unexposed women. Trends of increasing risk were also found with increasing duration of exposure to acids and caustics (p = 0.05), and with years worked in dyeing processes (p = 0.06). Women who worked at least 10 years in dyeing processes had a 3.6-fold excess risk of NPC (95% CI 1.0 to 12.1). CONCLUSIONS: Occupational exposure to cotton dust, acids, and caustics, and work in dyeing and printing jobs in the textile industry may have increased risk of NPC in this cohort.