Fatal cadmium-induced pneumonitis

VAHTER M. Fatal cadmium-induced pneumonitis. Scand J Work Environ Health 1993;19:429- 31. A previously relatively healthy 78-year old man was exposed to cadmium fumes during brazing with cadmium-containing silver solder. He developed severe chemical pneumonitis and died 25 d after exposure.

exa minatio n. His temperature wa s 38.3°C, hi s white blood cell count wa s 14 600 · mm', and the sedimentation rate was 75 mm· h-I . A che st X-ray re veal ed alveolar infiltrates on the base of the rig ht lung. The se find ings we re interpreted as pneumon ia, and the pat ient was gi ven penicill in Y, 2 g orally per day.
T wo days later, on 16 No vember, the patient returned with a sore throat and dyspnea. Hi s lip s we re cyanotic and the mu cous membranes in his throat were red and dry. At this point he expl ained that his co ugh appeared 3 h after brazing on stainless stee l. He was no w admitted to the hospital with the suspicion of having toxic pneumoniti s.
It was re vealed that, on II No vember , our patient and a friend had been manufacturing an apparatu s for the ille gal production of alcohol in his garage. Wh ile working, the patient had kept the metal pieces directly in front of him , without usin g any respirator y protecti ve equipment. Hi s friend had been bra zin g for about 15 min with a silver solde r, later an alyzed to contain 20-30% cadmium. The friend used respirator y protection during the br azing operation and was co nsequently less expo sed . The friend developed cough , shiveri ng, and fever, but felt we ll the ne xt morning and did not consult his physician.
When ad mitted to the ho spital on 16 No vember , the pat ient was initially tre ated in the intensive ca re uni t. His partial pressu re of arte rial ox ygen was 3.9 kP a, and he needed a Bird-mask the first 2 d, but his respiration did not have to be assisted in any oth er manner. He used his accessory breathin g mu scle s and had tachypnea and in spira tory rhonchi at auscultation. He was treated with oxygen and bronchodilato rs. He was not treated with steroids , as 5 d had passed since the ex pos ure. Benzylpenicillin (3 g) was given intravenously thre e times a day during the next 4 d.
On 20 November his ob stru ctive sympto ms became worse and an intraven ou s infusion containing 4 mg of bet amethasone and 15 ml oftheophyllamine was given twice daily during the next 5 d. The steroid treatm ent wa s incr ease d to 8 mg of betam ethason e, Scand J Work Environ Health 1993. vol 19, no 6 given intravenously four time s, without any significant effect.
The patient' s conditi on deteriorated slowly, and he died on 6 December due to respi ratory insufficiency. During the course of the illness his serum creatinine levels were 85, 124, 109 umol . 11; in other word s they were gen erally within the reference interval of 55-115 umol . 1-1 . Spirometry was not performed .

Autopsy
In the autop sy the patien t' s lungs were large and firm with the light micro scop ic appearance of extensive bron chopn eumonia and pronounced peribronchial, perivascular, and interstitial fibrosi s, a finding which may suggest that some of the changes were not caused by this acute intoxication. The patient's heart was slightly enlarged with no signs of recent or previou s infarction. The coronary arteri es were moderately arteriosclerotic. The kidneys wer e of normal size, somewhat granulated on the surface but with norm al color and consistency. Micro scopy was not performed for the kidne y. The liver was macro scopicall y normal.

Cadmium concentrations
The co ncentration of cadmium in the patient's blood was about 530 nmol . 1-1 at autopsy. His lungs contained 1.6 ug of cadmium per gram of wet weight (rang e of four samples 0.76-3.6 ug . g 1), the kidney corte x 23 ug . s' (range of four samples 20-26 f..Lg . g:'), and the liver 1.9 u g . s' (range of four samples 1.8-1.9 ug . g'), Cadm ium was determin ed with graphite furn ace atomic absorption spectrophotometry (6) at the Institute of Environmental Medicine, Karolinska Institute. The cadmium content of the solder was analyzed at the same laboratory.

Discussion
The brazer was expo sed to cadmium fumes giving rise to a blood level of 530 nmol . I-I, a value indi-eating significa nt exposure. Howe ver, postmortem blood samples should be int erpr eted with caution. With a half-time of about 100 d for the fast compartment of cadmium concentrations in blood (7 ), it can be estimated that the blood concentration at a time close to the exposure was about 630 nmol . I-I. In Sweden the median level of cadmium in blood among occupationally unexposed persons is about 2 nmol . II for nonsmokers and about 16 nmol . I-I for smokers (6). According to Swedish regu lations (8) , the blood concentration of cadmium should not exceed 100 nmol . 1-1amon g occupationally exposed subjects.
The conc entration of cadm ium in the lungs immediatel y after expo sure was probably higher than at the time of death . A rough figure , based on the est imated half-time in blood , would be about 1.9 g of cadmium per gram of lung tissue. As shown by table I, the con centration of cadmium in the lungs of our patient, as well as in all other reported cases leading to death , was clearly above the level of occupationally unexp osed men.
Lethal doses of cadmium fumes have been calculated to be 2600-2900 mg . rrr-' . min-I ( 13), for example , 260 mg . rrr' during 10 min or 8.6 mg . m" durin g 5 h, as reported by Beton et al (14). The se estimations are based on the measu red cadmium concentration, the weight of the lungs, the estimated retention of inhaled cadmium, and the respiratory minute volume. Information was lacking on the weight of the lungs of our patient. The time of soldering was 15 min , but the true exposure time was probably longer, as the patient spent time in the garage after the soldering acti vity.
Pulmonary fibrosis after a single expo sure to cadmium fum es has previously been reported by Townshend ( 15) . In 1963, a weld er developed pulmonary edema after welding a cadm ium-silver alloy ( 16). His lung function gradually improved durin g the first six months. Sevent een year s later this man developed severe progressive pulmonary fibrosis (15) .
A 30-year-old man work ed with silver solder for I h in a small, enclosed, unventilated tank. Later that Table 1. Concentrations of cadmium in lung , kidney, and liver from autopsies.

Lung
Kidney Liver Days Study (J!g. g-1 wet (J!g ' g-1 wet (J!g . g-1 wet after weight) weight) weight) exposure Occupationally unexposed men, 13-19" 0.5-1 .0 30-79 years of age (1, 9) 0. ne arly four years after the e xposure (17). A no the r man spent two weeks brazing th e propellers o f sh ips w ith a c ad mi um -c o n tain ing so lder in a c o nfined area with poor ve ntilation . He d e veloped f ib ro sing a lveo litis, w h ic h w as treated wi th predni solone. Hi s vital c ap acity was init ially 2. 8 I, but it improved gradually to 5.5 I after more th an a year (18 ).
Short-term exposure to hi gh le vel s of cad m iu m fum e s can c au se pulmonary ede ma a nd pneumoniti s . Pulmonary f ib rosi s is m ore se ldom reported after such exposure. In our ca se pneumonitis app eare d shortly after exposure and the man in question later developed re spiratory in su ffi cienc y , w h ic h w as th e c au se of de ath on e month aft e r exposure. Informati on o n th e true expo sure was probably del ayed due to th e illegal character of the pati ent' s activity. A n immediate sta rt of ste ro id treatment is important, and it mi ght have changed the outcome for thi s patient. This tragic case rep ort e m p hasi zes the ne ed for strict h ygi enic control measures w he never the hi ghly to xic m etal cad m iu m is handled.