(トリクロロメトキシ)ぎ酸クロリド

Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer for medical attention.

Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth.

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

Personal protection: chemical protection suit including self-contained breathing apparatus. Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations.

Burning sensation. Chest tightness. Sore throat. Cough. Laboured breathing. Shortness of breath. Symptoms may be delayed.

Redness.

Watering of the eyes. Redness.

Sore throat.

EYE IRRITATION, IRRITATION OF UPPER RESPIRATORY TRACT, & SURFACE BURNS HAVE BEEN PRINCIPAL FINDINGS IN EXPOSED HUMANS. PULMONARY EDEMA WOULD UNDOUBTEDLY OCCUR WITH HIGHER LEVELS OF EXPOSURE. EYE IRRITATION MAY PERSIST SOME TIME AFTER EXPOSURE CEASES. SKIN SENSITIZATION MAY OCCUR. /CHLOROFORMATES/

INSIDIOUS POISON AS IT IS NOT IRRITATING IMMEDIATELY, EVEN WHEN FATAL CONCN ARE INHALED. MAY CAUSE SEVERE PULMONARY EDEMA (MAY BE QUICKLY FATAL) OR PNEUMONIA. INHALATION OF HIGH CONCN CAUSES CHOKING, CONSTRICTED FEELING IN CHEST, COUGHING, PAINFUL BREATHING, BLOODY SPUTUM. VAPORS STRONGLY IRRITATING TO THE EYES. /PHOSGENE/

HIGHLY TOXIC BY INHALATION & INGESTION. STRONG IRRITANT TO TISSUE.

NO EVIDENCE EXISTS FOR A SYSTEMIC ACTION OF INHALED PHOSGENE, BUT VASOCONSTRICTION OF PULMONARY VASCULATURE HAS BEEN DESCRIBED IN RABBITS. SEQUELAE INCLUDE PULMONARY SCARRING, LOBULAR EMPHYSEMA, SMALL IRREGULAR AREAS OF ATELECTASIS & BRONCHITIS. /PHOSGENE/

SOME POSSIBLE MECHANISMS OF REDUCED ACTIVITY OF LUNG SURFACTANT IN ACUTE PULMONARY EDEMA WERE STUDIED IN ALBINO RATS & RABBITS. MOST OF THE EDEMOGENIC SUBSTANCES DID NOT CHANGE SURFACTANT ACTIVITY WHILE DIPHOSGENE REDUCED IT.

The purpose of this study was to examine the changes of pulmonary hemodynamics, cardiac impedance parameters and the number of pulmonary microembolus, and leukocyte after diphosgene inhalation in rabbits. Fifty-three rabbits were randomized into two sets, one set was used to monitor the pulmonary hemodynamics, the other set was used to determine the cardiac impedance parameters, microemboli and leukocytes were obtained directly from the pulmonary microcirculation by use of the retrograde perfusion method. As compared with control group, lt was found that pulmonary artery pressure rose and pulmonary vascular resistance increased (p < 0.05), but did not correlate with lung water parameters (p > 0.05). At 1, 6 hr after diphosgene inhalation cardiac Impedance parameters did not change (p > 0.05~, as compared with before inhalation. Microemboli (21.8 increased (p< 0.05), as compared with the control group (106/L, 430e pulmonary hemodynamics, but could not effectively reduce the degree of pulmonary edema.