Exposure to toxic fumes from an industrial chemical fire may not only lead to airway burns and inhalational injury but also toxic exposure via the transdermal route.

A 45-year-old gentleman presented with dyspnea two hours after a ten-minute exposure to toxic fumes while fighting an industrial chemical fire without personal protective equipment. He reported voice hoarseness and chest tightness. Nasoendoscopy demonstrated paranasal sinus soot and significant upper airway edema. Awake fiber-optic intubation was performed for prophylactic airway protection in the Burns ICU but bronchoscopy did not reveal any inhalational burns.

However, the patient developed worsening lactic acidosis (serum lactate 2.8mmol/L to 8.1mmol/L with pH 7.28) within 12 hours post-exposure. Carboxyhemoglobin was 0.9%. Toxicology was consulted for suspicions of transdermal HAZMAT contamination, in particular cyanide given the profound lactic acidosis. The patient was given two doses of hydroxocobalamin and brought to the Hospital Decontamination Unit for de-gowning and thorough wash-down. The chemical scan meter showed high levels (352IU) of an unknown chemical on his skin pre-decontamination, which could not be detected post-decontamination. Lactate improved to 5.0mmol/L within two hours post-decontamination while acidosis resolved at eight hours post-decontamination. The patient was extubated and discharged without sequelae.

To our knowledge, no other human cases of transdermal cyanide poisoning have been reported. Cyanide interferes with mitochondrial oxidative phosphorylation pathways to cause toxicity and death if untreated. However, its effects via transdermal exposure are often delayed compared to exposure via more conventional inhalational routes. This makes recognition difficult and compounds the challenge of long turnaround time for blood cyanide tests. Increased transdermal absorption is possible through intact skin if moistened by sweat.

The potential for transdermal HAZMAT absorption from exposure to toxic fumes is underrecognized. It is crucial to maintain vigilance given the challenges in diagnosing transdermal cyanide toxicity and importance of initiating treatment early.

Few studies have prospectively examined psychosocial and psychiatric predictors of adolescent substance use disorders simultaneously.

To identify psychosocial and psychiatric predictors of substance use disorders in adolescence.

School children aged 12 years (s. d. =0. 3) free from any substance use disorder at grade7(n=428) were assessed in three consecutive years, using a standardised psychiatric interview. Their baseline psychosocial information was also collected. The outcome was the onset age of a substance use disorder. The Cox regression model was used for data analysis.

The most significant predictive factors for adolescent substance use disorder included male gender, attention-deficit hyperactivity disorder, conduct disorder and sibling use of tobacco. Three protective factors against such morbidity included living in a household with two parents, a good academic grade at grade 7 and objection to the use of substances.

Early intervention for disruptive behaviour disorders and specific psychosocial risk factors might prevent substance use disorders in early adolescence.