OBJECTIVETo determine the cause of acute poisoning occurred in a factory in Yangjiang city, Guangdong province.

METHODSIn a cross-sectional study, interviews were conducted with the administrators of the factory and the local physician. A review was conducted on the water system used for industrial purposes and a separate system used by workers for drinking water. Treatment and discharge of industrial waste water were examined. Face-to-face interview was conducted to identify risk of exposure for illness among workers.

RESULTSA total number of 36 cases were identified in the plant and the attack rate was 16.4% (36/220). The incubation period (time between drinking polluted water and the onset of symptoms) had a median of 90 minutes (range: 30 - 230 minutes). Consuming water at the factory increased the attack rate and a dose-response effect was identified (chi(2)(trend) = 79.115, P < 0.01). The nitrite content of residuals in drinking water exceeded the WHO standard (1 ppm).

CONCLUSIONSThe accident of acute poisoning was due to drinking water contaminated with sodium nitrite. The prevention of drinking water contaminated by toxic chemicals like sodium nitrite, and the design of industrial and potable water supply system need to be carefully reviewed. Regulations should be developed and enforced to minimize the impact of industrial waste water discharges to guarantee the access to clean drinking water.

Acute Disease ; Adolescent ; Adult ; Female ; Humans ; Industrial Waste ; Male ; Middle Aged ; Nitrites ; poisoning ; Water Pollutants, Chemical ; poisoning ; Water Supply ; analysis

Many human genetic diseases, including Hutchinson-Gilford progeria syndrome (HGPS), are caused by single point mutations. HGPS is a rare disorder that causes premature aging and is usually caused by a de novo point mutation in the LMNA gene. Base editors (BEs) composed of a cytidine deaminase fused to CRISPR/Cas9 nickase are highly efficient at inducing C to T base conversions in a programmable manner and can be used to generate animal disease models with single amino-acid substitutions. Here, we generated the first HGPS monkey model by delivering a BE mRNA and guide RNA (gRNA) targeting the LMNA gene via microinjection into monkey zygotes. Five out of six newborn monkeys carried the mutation specifically at the target site. HGPS monkeys expressed the toxic form of lamin A, progerin, and recapitulated the typical HGPS phenotypes including growth retardation, bone alterations, and vascular abnormalities. Thus, this monkey model genetically and clinically mimics HGPS in humans, demonstrating that the BE system can efficiently and accurately generate patient-specific disease models in non-human primates.
Animals ; Disease Models, Animal ; Female ; Gene Editing ; Humans ; Lamin Type A/metabolism* ; Macaca fascicularis ; Progeria/pathology*